Received: 23 February 2018
Accepted: 28 June 2018
Evidence of curcumin and curcumin analogue effects in skin
diseases: A narrative review
Stephen L. Atkin
Alexandra E. Butler
Thomas P. Johnston
Chemical Injuries Research Center, Systems
Biology and Poisonings Institute, Baqiyatallah
University of Medical Sciences, Tehran, Iran
Department of Chemistry, Faculty of Science,
K. N. Toosi University of Technology, Tehran, Iran
Weill Cornell Medicine Qatar, Doha, Qatar
Sabinsa Corporation, East Windsor, New Jersey
Life Sciences Research Division, Anti‐Doping
Laboratory Qatar, Doha, Qatar
Division of Pharmaceutical Sciences, School
of Pharmacy, University of Missouri‐Kansas
City, Kansas City, Missouri
Biotechnology Research Center, Pharmaceutical
Technology Institute, Mashhad University of
Medical Sciences, Mashhad, Iran
Neurogenic Inflammation Research Center,
Mashhad University of Medical Sciences,
School of Pharmacy, Mashhad University of
Medical Sciences, Mashhad, Iran
Omid Fazlolahzadeh, Department of Chemistry,
Faculty of Science, K. N. Toosi University of
Technology, 16315‐1618, Tehran, Iran.
Amirhossein Sahebkar, Department of Medical
Biotechnology, School of Medicine, Mashhad
University of Medical Sciences, Mashhad
Curcumin, a natural polyphenolic and yellow pigment obtained from the spice turmeric, has
strong antioxidative, anti‐inflammatory, and antibacterial properties. Due to these
properties, curcumin has been used as a remedy for the prevention and treatment of
skin aging and disorders such as psoriasis, infection, acne, skin inflammation, and skin
cancer. Curcumin has protective effects against skin damage caused by chronic ultraviolet
B radiation. One of the challenges in maximizing the therapeutic potential of curcumin is its
low bioavailability, limited aqueous solubility, and chemical instability. In this regard, the
present review is focused on recent studies concerning the use of curcumin for the
treatment of skin diseases, as well as offering new and efficient strategies to optimize its
pharmacokinetic profile and increase its bioavailability.
curcumin, dermatology, inflammation, skin, topical use
J Cell Physiol. 2018;1–14. wileyonlinelibrary.com/journal/jcp © 2018 Wiley Periodicals, Inc.
Abbreviations: 5‐LOX, 5‐lipoxygenase; AAPK, autophosphorylation‐activated protein kinase; AATF‐1, arylamine N‐acetyltransferases 1; AHR, aryl hydrocarbon receptor; AP‐1, activating
protein 1; AR, androgen receptor; Bcl‐2, B‐cell lymphoma protein 2; Ca
‐dependent protein kinase; CKCR4, chemokine (C‐X‐C motif) receptor 4; COX‐2, cyclooxygenase 2; CREB‐BP,
CREB‐binding protein; CTGF, connective tissue growth factor; DFF‐40, DNA fragmentation factor 40 kDa subunit; DNA Pol, DNA polymerase; DR5, death receptor 5; EGF, epidermal growth
factor; EGFR, EGF receptor; EGF‐RK, EGF receptor kinase; ELAM‐1, endothelial leukocyte adhesion molecule 1; EPCR, endothelial protein C receptor; ERE, electrophile response element; ERK,
extracellular receptor kinase; ER‐α, estrogen receptor‐α; FAK, focal adhesion kinase; FGF, fibroblast growth factor; FPT, farnesyl protein transferase; FR, Fas receptor; GCL, glutamyl cysteine
ligase; GST, gluthathione‐S‐transferase; H2R, histamine (2) receptor; HER‐2, human epidermal growth factor receptor 2; HGF, hepatocyte growth factor; HIF‐1, hypoxia‐inducible factor 1; HO,
hemeoxygenase 1; HSP‐70, heat‐shock protein 70; IAP‐1, inhibitory apoptosis protein 1; ICAM‐1, intracellular adhesion molecule 1; IL‐1, interleukin 1; IL‐12, interleukin 12; IL‐18, interleukin
18; IL‐1R AK, IL‐1 receptor‐associated kinase; IL‐2, interleukin 2; IL‐5, interleukin 5; IL‐6, interleukin 6; IL‐8 R, interleukin 8 receptor; IL‐8, interleukin 8; iNOS, inducible nitric oxide synthasel;
IR, integrin receptor; JAK, janus kinase; JNK, c‐jun N‐terminal kinase; LDLR, low density lipoprotein‐receptor; MaIP, macrophage inflammatory protein; MAPK, mitogen‐activated protein
kinase; MCP, monocyte chemoattractant protein; MDRP, multidrug resistance protein; MIP, migration inhibition protein; MMP, matrix metalloproteinase; NF‐κB, nuclear factor κ‐light‐chain‐
enhancer of activated B cells; NGF, nerve growth factor; NQO‐1, NAD(P)H: quinoneoxidoreductase 1; Nrf, nuclear factor 2‐related factor; ODC, ornithine decarboxylase; PAK, protamine
kinase; PCNA, proliferating cell nuclear antigen; PDGF, platelet‐derived growth factor; PhPD, phospholipase D; PKA, protein kinase A; PKB, protein kinase B; PKC, prorein kinase C; Pp60c‐tk,
pp60c‐src tyrosine kinase; PPAR‐γ, peroxisome preoliferator‐activated receptor‐γ; PTK, protein tyrosine kinase; Src‐2, Src homology 2 domain‐containing tyrosine phosphatase 2; STAT‐1,
signal transducers and activators of transcription 1; STAT‐3, signal transducers and activators of transcription 3; STAT‐4, signal transducers and activators of transcription 4; STAT‐5, signal
transducers and activators of transcription 5; TF, tissue factor; TGF‐β1, transforming growth factor‐β1; TMMP‐3, tissue inhibitor of metalloproteinase 3; TNFα, tumor necrosis factor α; uPA,
urokinase‐type plasminogen activator; VCAM‐1, vascular cell adhesion molecule 1; VEGF, vascular endothelial growth factor; WTG‐1 , Wilms’tumor gene 1.
This review focuses on curcumin, the compound that imparts the yellow
color to turmeric and that is used to flavor food. For centuries, turmeric
has been used as a remedy for multiple conditions including dyspepsia,
liver disorders, flatulence, jaundice, urinary tract diseases, colds, biliary
disorders, rheumatism, sinusitis, chronic otorrhea, diabetic ulcers, cough,
and various skin conditions (Hewlings & Kalman, 2017). Turmeric
possesses more than 300 different components, including phenolic
compounds and terpenoids (B. B. Aggarwal, Yuan, Li, & Gupta, 2013).
Turmeric contains three naturally occurring curcuminoids: Curcumin or
diferuloylmethane (75%), demethoxycurcumin (20%), and bisdemethox-
ycurcumin (5%; Akbik, Ghadiri, Chrzanowski, & Rohanizadeh, 2014).
Chemically, curcumin is a lipophilic molecule (1,7‐bis(4‐hydroxy3‐
methoxyphenyl)‐1,6‐heptadiene‐3,5‐dione) and a natural polyphenol. Its
chemical structure includes keto‐enol tautomerism (depending on
whether curcumin resides in an acidic or alkaline medium). The molecule
rapidly permeates cell membranes and acts on multiple targets in various
cellular pathways to elicit various therapeutic actions in a variety of
diseases. Due to variable efficacy and the side effect profiles of many
modern medications, it is an appropriate time to assess the therapeutic
usefulness of ancient and traditional medications, including curcumin
(Kocaadam & Sanlier, 2017). Curcumin’s simple molecular structure,
along with its varied therapeutic effectsanditsuseinmanydisease
conditions has attracted much attention (Cheppudira et al., 2013;
Kunnumakkara et al., 2017). Curcumin can be used as an effective
treatment in several diseases by targeting different molecular targets and
with minimal toxicity to both humans and animals (Cheppudira et al.,
2013; Kocaadam & Sanlier, 2017; Kunnumakkara et al., 2017).
Curcumin is well known to exert therapeutic effects against a variety
of pathological conditions including cancer (Iranshahi et al., 2010;
Momtazi et al., 2016; Teymouri, Pirro, Johnston, & Sahebkar, 2017),
chemotherapy‐induced adverse reactions (Mohajeri & Sahebkar, 2018;
Rezaee, Momtazi, Monemi, & Sahebkar,2017),metabolicsyndrome
(Panahi et al., 2015; Panahi, Khalili, Hosseini, Abbasinazari, & Sahebkar,
2014), osteoarthritis (Panahi, Rahimnia, et al., 2014; Sahebkar & Henrotin,
2016), dyslipidemias (Cicero et al., 2017; Ganjali et al., 2017; Sahebkar,
2014; Sahebkar et al., 2016; Simental‐Mendia et al., 2017), diabetes
(Hajavi et al., 2017; Panahi et al., 2017, 2018), nonalcoholic fatty liver
disease (Rahmani et al., 2016), endothelial dysfunction (Karimian, Pirro,
Johnston, Majeed, & Sahebkar, 2017), hyperuricemia (Panahi et al., 2016),
respiratory diseases (Lelli, Sahebkar, Johnston, & Pedone, 2017; Panahi,
Ghanei, Bashiri, Hajihashemi & Sahebkar, 2015; Panahi, Ghanei,
Hajhashemi & Sahebkar, 2016), and autoimmune diseases (Abdollahi,
Momtazi, Johnston, & Sahebkar, 2018; Momtazi‐Borojeni et al., 2018).
According to the literature, turmeric has been orally and topically used in
the prevention and treatment of skin diseases, which include parasitic
skin infections, infected wounds, premature aging, inflammation, and
psoriasis (Vaughn, Branum, & Sivamani, 2016).
Skin is the largest organ of the human body and is responsible for
covering, separating, and protecting the body from the external
environment, receiving sensory stimuli, and regulating body
temperature. Premature aging of the skin may be related to extrinsic
factors and personal lifestyle choice such as smoking, solar radiation
exposure, low air humidity, poor diet, and excess alcohol intake, as
well as systemic diseases such as diabetes mellitus. According to the
literature, curcumin possesses significant therapeutic effects for
various skin conditions, including anti‐inflammatory properties (B. B.
Aggarwal et al., 2013), ultraviolet (UV) protection (H. Li et al., 2016),
antioxidant effects (Xie et al., 2015), chemopreventive and che-
motherapeutic activity (Jiang, Jiang, Li, & Zheng, 2015; Lelli, Pedone,
& Sahebkar, 2017; Qiu et al., 2014; Toden et al., 2015), wound
healing benefits (Akbik et al., 2014), and antimicrobial effects (Krausz
et al., 2015). Due to its free‐radical scavenging and anti‐inflammatory
properties, topical application of curcumin has allowed new
therapeutic avenues for wound healing, protection against oxidative
skin damage, skin cancer treatment (Qiu et al., 2014), control of pain
resulting from dermal burns (J. Kim et al., 2016; Mehrabani et al.,
2015), androgen‐dependent skin disorders (Liao et al., 2001), and
decreasing skin irritation and reducing the symptoms of autoim-
mune‐related skin disorders such as psoriasis (Kang et al., 2016).
However, recent studies have highlighted curcumin’s poor
bioavailability, low aqueous solubility, chemical instability, rapid
degradation, and rapid systemic elimination as major limitations for
its use in clinical practice (Kharat, Du, Zhang, & McClements, 2017).
This review aims to provide recent evidence for the usefulness of
curcumin in dermatology, as well as to suggest strategies to increase
its effectiveness and stability in vivo.
Exposure of human skin to solar radiation, chemical pollutants, and
mechanical stress results in the generation of free radicals. Free
radicals, like reactive oxygen species (ROS), are unstable chemical
entities that are highly reactive, cause skin damage through
inflammation, and may result in skin cancer. The resultant destruc-
tion of proteins, collagen, and elastic fibers is reflected in the signs of
skin aging (Poljsak & Dahmane, 2012). Antioxidants are compounds
that are protective by quenching free radical activity. The antioxidant
system in the skin includes superoxide dismutases (SOD), catalases,
and peroxidases (selenium‐dependent glutathione peroxidases [GPx],
for example). Aging and prolonged exposure to ROS‐generating
factors, which include poor nutrition, alcohol intake, UV radiation,
stress, and environmental pollution, result in ROS accumulation,
which in turn damages the skin (Lee et al., 2013).
While most of the antioxidants have either a phenolic functional
group or a‐diketone group, there are different functional groups including
the B‐diketo group, carbon–carbon double bonds, and phenyl rings
containing varying amounts of hydroxyl and methoxy entities that make
curcumin a unique and potent antioxidant. Curcumin’s antioxidant
activity is attributed to its diketone and phenol moieties (diferuloyl‐
methane portion of the molecule), which are free radical quenchers (Lee
et al., 2013). Masuda et al. (2001) proposed that the antioxidant
PANAHI ET AL.
mechanism of curcumin includes an oxidative coupling reaction at the 3ʹ
position of the curcumin structure with lipid and a subsequent
intramolecular Diels–Alder reaction. Curcumin functions as a mediator
in the regulation of genes related to the generation of proteins with
antioxidant characteristics such as heme oxygenase‐1, transcription and
growth factors, and inflammatory cytokines (Kou et al., 2013; O’Toole
et al., 2016). Curcumin also regulates antioxidant enzymes, scavenges
hyperglycemia‐induced ROS, and profoundly increases the intracellular
antioxidant, reduced glutathione (GSH), which serves to decrease lipid
peroxidation. Studies have also shown strong protective effects of
curcumin against damage to the keratinocytes and fibroblasts in the skin
induced by H
(Phan, See, Lee, & Chan, 2001). Tetrahydrocurcumi-
noids obtained by hydrogenating cucuminoids (Prakash & Majeed, 2009)
are one of the major colorless metabolites of curcumin, in the form of its
glucuronide conjugate in bile. This conjugate compound has been shown
to have enhanced antioxidant properties with superior free radical
scavenging, free radical formation prevention, and increased lipid
peroxidation inhibition compared to curcumin and vitamin E (Prakash &
Therefore, the literature suggests that curcumin and its deriva-
tives may be promising and effective antioxidants that can be used
both orally and topically.
ANTI‐INFLAMMATORY AND WOUND
Acute and chronic inflammation are part of the body’s defense
mechanisms and involve immune cells, blood vessels, and molecular
mediators in response to harmful stimuli such as pathogens or
irritants. Pain, redness, immobility, swelling, and heat are the
hallmark signs of skin inflammation. Cytokines and hormone‐like
polypeptide mediators like tumor necrosis factor α(TNF‐α, a key
proinflammatory cytokine) induce proinflammatory cytokines such as
interleukins 1, 6, 8, 10, and 21 and result in the activation of nuclear
factor κ‐light‐chain‐enhancer of activated B cells (NF‐κB), c‐Jun
‐terminal kinase, and mitogen‐activated protein kinase (MAPK)
in the skin. These factors play a major role in the pathogenesis of
many inflammatory skin diseases and in the immunoregulatory
responses. Most inflammatory skin disorders are associated with
the overproduction of cytokines, dysregulation of cytokines, or
alterations in cytokine receptors (Figure 1).
Curcumin’santi‐inflammatory properties have been unequivocally
established (R. Agrawal, Sandhu, Sharma, & Kaur, 2015; Koop, de Freitas,
de Souza, Savi, & Silveira, 2015) in several different organs such liver and
skin through modulation of autoimmune disease and prevention of injury
to these organs–tissues (R. Agrawal et al., 2015). The primary mechanism
by which curcumin modulates inflammation is by reducing the expression
of the two main cytokines that are released by monocytes and
macrophages (Figure 1; Akbik et al., 2014; Kang et al., 2016). These
molecules are interleukin 1 (IL‐1) and TNF‐α, which have important roles
in the regulation of the inflammatory response. Also, curcumin inhibits
the activity of the proinflammatory transcriptional factor, NF‐κB, which is
responsible for the regulation of many genes involved during the initial
onset of the inflammatory response. A variety of kinases (AKT, PI3K, and
IKK) activate NF‐κB (Jagetia & Rajanikant, 2015). Suppression of NFκB
activation causes downregulation of cyclooxygenase‐2andinducible
nitric oxide synthase, and prevents upregulation of vascular endothelial
FIGURE 1 Activation of NF‐κB plays a
major role in the pathogenesis of many
inflammatory skin diseases. NF‐κB: nuclear
factor κ‐light‐chain‐enhancer of activated
B cells [Color figure can be viewed at
PANAHI ET AL.
growth factor (VEGF) messenger RNA and microvascular angiogenesis
during inflammatory conditions. Curcumin’santi‐inflammatory actions
can be utilized to control inflammation of the skin resulting from different
skin diseases. For example, Arunraj et al. (2014) studied the anti‐
inflammatory actions of curcumin and curcumin nanospheres (CNSs) to
prevent denaturation of bovine serum albumin and compared it with
diclofenac sodium (a nonsteroidal anti‐inflammatory drug) both in vitro
and ex vivo. The results of in vitro stability testing for heat‐treated
albumin at physiological pH showed that CNSs had a greater anti‐
inflammatory effect in comparison with curcumin and diclofenac across a
dose range (25–1,000 μg/ml).
Skin is an essential protective organ for the body against the
environment. Chronic injuries in skin cause the body to initiate a
dynamic and multistep process of repair to regain tissue integrity. Four
processes are involved during the wound healing process: hemostasis,
inflammation, proliferation, and remodeling (Hussain, Thu, Ng, Khan, &
Katas, 2017; Margolis et al., 2011). At the initiation of the injury, rapid
aggregation of platelets via hemostasis causes clot formation. Migration
of neutrophils and macrophages to the wound site and release of
cytokines, thereby promoting fibroblast migration, results in inflamma-
tion at the wound site. Re‐epithelialization, generation of new blood
vessels (termed angiogenesis or neovascularization), and extracellular
matrix protein deposition by fibroblasts (collagen fibers, granulation
tissue, for example) occur to protect cell ingrowth. Collagen is used as
the building block during this proliferation phase (Hussain et al., 2017;
Margolis et al., 2011). The collagen remodeling and formation of scar
tissue is the final phase of wound healing. Inflammation, part of the acute
injury response, attracts neutrophils to the injured site resulting in the
release of inflammatory mediators such as TNF‐αand IL‐1(Arunrajetal.,
2014). Neutrophils in the wound area are associated with high levels of
destructive proteases and ROS molecules, which cause inflammation and
result in tissue damage, as well as prolonging the inflammatory phase.
The ROS molecules, bacterial infection, and protracted inflammation are
the major reasons for delays in wound healing (Guo & Dipietro, 2010;
Sorg, Tilkorn, Hager, Hauser, & Mirastschijski, 2017). Therefore,
curcumin’s potent antioxidant, anti‐inflammatory, and anti‐infectious
actions can play a healing role in the process of wound resolution (Akbik
et al., 2014; Mohanty & Sahoo, 2017). Topical application of curcumin
has been shown to promote re‐epithelialization in burn wound areas to
increase the rate of wound healing (Kulac et al., 2013; Lopez‐Jornet,
Camacho‐Alonso, Jimenez‐Torres, Orduna‐Domingo, & Gomez‐Garcia,
2011). Clinical studies have indicated an increased rate of epidermal
growth, increased thickness of the cuticular layer, and significant
improvement in wound healing in curcumin‐treated subjects when
compared to untreated subjects (Kulac et al., 2013; J. Li, Chen, & Kirsner,
2007; Wen, Wu, Chen, Yang, & Fu, 2012).
Kulac et al. (2013) reported that topical treatment with curcumin at a
concentration of 100 mg/kg body weight on burn wound healing in rats
enhanced the healing process compared to the control group, with a
decrease in inflammatory cells, and enhanced collagen deposition,
angiogenesis, granulation tissue formation, and epithelialization. Castan-
gia et al. (2014) used curcumin nanovesicles for wound healing in chronic
cutaneous pathologies in both in vivo and in vitro studies. They showed
that nanoentrapped curcumin prevented the formation of skin lesions
and inhibited the biochemical processes that normally lead to epithelial
damage. Based upon epidemiological evidence, they recommended the
daily topical application of curcumin‐loaded nanovesicles for patients at a
higher risk of skin wound infection to afford better protection. Using
liposomes and penetration enhancer-containing vesicles (PEVs) showed
an additional benefit by enhancing skin penetration. Krausz et al. (2015)
showed that topical use of curcumin‐encapsulated nanoparticles in an in
vivo murine wound model enhanced granulation tissue, re‐epithelializa-
tion and decreased wound area after 14 days of treatment leading to
improved wound healing. The results showed statistically significant
acceleration of wound healing in mice treated with curcumin‐encapsu-
lated nanoparticles (curc‐np) compared to untreated, silver sulfadiazine,
coconut oil, control, control np, and curcumin (curc). Topical curcumin
used in breastfeeding women suffering lactation‐induced mastitis showed
that curcumin effectively decreased mastitis‐related pain, breast tender-
ness, and erythema. This reduction in inflammation occurred within 72 hr
of administration without any side effects showing the efficacy of
curcumin in this situation (Afshariani, Farhadi, Ghaffarpasand, &
Psoriasis is an epidermal hyperproliferative and autoimmune dermal
chronic inflammatory disease caused by genetic and immunologic
factors and normally affects the skin and joints (Lowes, Suarez‐Farinas,
& Krueger, 2014). Psoriasis shows triggering of intraregional
T‐lymphocytes that prime basal stem keratinocytes to proliferate
excessively. Enhanced cell proliferation results in an excessive buildup
of cells on the surface of the skin and rapidly forms scales and red
patches that are itchy, inflamed, and sometimes painful. External
triggers like stress, alcohol, injury, infection, and medications may
initiate new psoriasis lesions. Psoriasis initiates from the premature
maturation of keratinocytes induced by an inflammatory cascade in the
dermis by dendritic cells, macrophages, and T cells. These immune cells
move from the dermis to the epidermis and secrete inflammatory
chemical signals (cytokines) such as IL 36‐γ,interferon‐γ(IFN‐γ), TNF‐α,
IL‐17, IL‐6, IL‐8, and IL‐22, that stimulate keratinocytes to proliferate.
Consequently, skin cells are replaced every 3–5 days rather than the
usual 28–30 days, resulting in scales on the surface of skin.
Reports suggest that the anti‐inflammatory effect of curcumin
may allow it to act as an antipsoriasis agent (H. Liu, Danthi, &
Enyeart, 2006; Sun et al., 2017). Some reports on the inhibitory
activity of curcumin suggest that its action on the potassium
channel subtype Kv1.3 in T cells plays a central role in psoriasis
(Kang et al., 2016; H. Liu et al., 2006). Recently, Kang et al. (2016)
showed that generation of T‐cell inflammatory factors, such as
IL‐17, IL‐22, IFN‐γ,IL‐2, IL‐8, and TNF‐α,decreasedby30–60% in
mice with psoriasis‐like diseases after 20 days of oral curcumin.
Over 50% of T‐cell proliferation was interrupted by application
of a 100‐μM curcumin preparation, and curcumin significantly
decreased the signs of psoriasis and improved the condition of the
PANAHI ET AL.
skin. Curcumin (10 μM) reduced the generation of inflammatory
agents (IL‐17, IL‐22, IFN‐γ,IL‐2, IL‐8, and TNF‐α)invitroin
Tcellsby30–60%. Sun et al. (2017) studied different formulations
of curcumin (dose: 0.25 mg·day
) and tacrolimus (dose:
) on the imiquimod (IMQ)‐induced psoriasis‐
like mouse model both in vitro and in vivo, compared to a placebo
vehicle as control. Their results showed that treatment using
tacrolimus and 50 nm Cur‐NPs gel reduced the white scale
thickness and the pink hue in inflamed skin. Also, they demon-
strated that encapsulation of curcumin into a poly(lactic‐co‐
glycolic) acid (PLGA)‐based nanoparticle‐containing hydrogel fa-
cilitated penetration through the skin and into the circulation (Sun
et al., 2017). In fact, this formulation had a superior performance
when compared to curcumin hydrogel in this imiquimod (IMQ)‐
induced psoriasis‐like mouse model, significantly improving the
antipsoriasis activity of curcumin.
Solar radiation induces both an acute and chronic reaction in animal and
human skin. One of the most important agents causing ROS production in
the body is UVB irradiation, which causes oxidative modification of
cellular lipids, proteins, and nucleic acids and can lead to inflammation,
gene mutation, and immunosuppression (Dupont, Gomez, & Bilodeau,
2013; Natarajan, Ganju, Ramkumar, Grover, & Gokhale, 2014). High
levels of UV radiation kill most of the skin cells in the upper skin layer,
and cells that are not killed are damaged. In its mildest form, sunburn
leads to erythema on skin; however, severe sunburn may cause the skin
to blister and peel, which is not only painful but also leaves the new skin
unprotected and more prone to UV damage. Excessive UV radiation
damages the skin’s cellular DNA, producing genetic mutations that can
lead to precancers like actinic keratoses, and to skin cancers including
melanoma. UVB (290–320 nm) radiation is highly mutagenic and
carcinogenic in animal experiments compared to UVA (320–400 nm)
Recently, several research groups have studied curcumin’s
protective effects against skin damage caused by chronic UVB
irradiation (Khandelwal et al., 2016). They showed that curcumin
exhibited photoprotective activity against acute UVB irradiation‐
induced photo damage. Topical application of curcumin before
chronic UV irradiation delayed the appearance of dermal tumors,
inflammation, and skin aging. H. Li et al. (2016) demonstrated that
short‐term topical application of emulsified curcumin (2 mg/ml
curcumin was prepared in 0.5% carboxymethyl cellulose sodium
[CMC‐Na]) protected against acute UVB irradiation‐induced
inflammation and photoaging‐associated damage in mouse skin
without any adverse effects. They show that curcumin attenuated
lactate dehydrogenase release induced by acute UVB irradiation in
HaCaT cells. The photoprotective effect of curcumin can be
attributed to its antioxidant properties and inhibition of UVB‐
induced oxidative damage by regulating the Nrf2 signaling path-
way in mouse skin and HaCaT cells (Khandelwal et al., 2016; H. Li
et al., 2016). Curcumin inhibited the generation of metallopro-
teases and NF‐κB in human dermal fibroblasts, which play a key
role in UVB exposure‐induced skin damage.
Chopra et al. (2016) encapsulated curcumin with a biodegradable
polymer, PLGA (150 nm size range), and termed this formulation–
preparation PLGA‐Cur‐NPs. They studied the protective effect of
curcumin in mouse fibroblasts (NIH‐3T3) and human keratinocytes
(HaCaT) against UV rays in vitro. They demonstrated sustained
release of curcumin at a low level from the PLGA‐Cur‐NPs and
suggested that this formulation could be an effective agent to protect
skin from exposure to UV irradiation. The results of this study
suggest that slow release of curcumin from PLGA‐Cur‐NPs could
counteract the adverse effects of photodegradation on curcumin
formulations upon exposure to UVA and UVB irradiation. UVB
exposure can induce cyclobutane pyrimidine dimers, leading to DNA
damage and skin cancer. According to various studies, considerable
DNA damage occurred with free curcumin, whereas this was not the
case with PLGA‐Cur‐NPs (Chopra et al., 2016).
Preclinical studies (Elad et al., 2013; H. Kim, Park, Tak, Bu, & Kim, 2014;
Kuttan, Sudheeran, & Josph, 1987; Phillips et al., 2013, 2011) on
curcumin have established its anticancer properties in breast, cervical,
skin, and pancreatic cell lines. However, rapid systemic clearance, low
aqueous solubility, poor physicochemical stability, and low cellular
uptake have limited the applications of curcumin. Recently, use of
nanotechnology for encapsulation of curcumin has improved its
therapeutic index, delivery, and bioavailability (Mangalathillam et al.,
2012). One of the most lethal skin cancers is melanoma, a result of
carcinogenic transformation of melanocytes (the pigment‐containing
cells of the skin). The DNA damage caused by UV light exposure is
central to the development of melanoma in people with low levels of
skin pigment (Autier & Dore, 1998). Studies showed that cytokine
expression can support the growth and metastasis of melanoma cells.
Elias et al. reported that over 80% of human melanoma cell lines
produce excessive levels of several cytokines and growth factors, such
as transforming growth factor β(TGF‐β), IL‐8, IL‐6, IL‐1α, VEGF, platelet‐
derived growth factor‐AA, and osteopontin (OPN), that are capable of
stimulating tumor growth, invasion, and angiogenesis.
Jiang et al. (2015) studied the human melanoma cell lines A375, MV3,
and M14 and the human normal lung fibroblast cell line MRC‐5invitro,
and showed that the viability of melanoma cells decreased with
increasing concentrations of curcumin from 5 to 50 μm. They demon-
strated that curcumin suppresses proliferation and induces double strand
break, suppressing the activation of NF‐κB (involved in tumor cell
proliferation) and causing apoptosis in melanocytes. Curcumin also
suppresses B‐cell lymphoma protein 2 (Bcl‐2) and myeloid cell leukemia‐1
(Mcl‐1) expression and upregulates the expression of Bax (a p53), which
are primary drivers for apoptosis. Following curcumin treatment, the
t‐bax to Bcl‐2 ratio increased, demonstrating that curcumin induced
apoptosis. The regulation of Bax, Bcl‐2, and Mcl‐1 expressions indicates
PANAHI ET AL.
that mitochondrial pathways play a key role in curcumin‐induced
apoptosis; thus, curcumin may provide antitumor efficacy and may offer
hope to those with melanoma. Additionally, Huang et al. (1997) showed
that topical application of very low doses (1–3,000 nM) of curcumin on
mouse epidermis inhibited the mean values of the 12‐O‐tetradecanoyl-
phorbol‐13‐acetate‐induced epidermal oxidized DNA base 5‐hydroxy-
methyl‐29‐deoxyuridine and, hence, tumor promotion. Jose, Labala,
Ninave, Gade, and Venuganti (2018) studied the synergistic effect of
encapsulated curcumin in 1,2-dioleoyl-3-trimethylammonium-propane
(DOTAP)‐based cationic liposomes, as well as complexed with signal
transducers and activators of transcription 3 (STAT‐3) small interfering
RNA (siRNA); they demonstrated that in an animal model of melanoma
skin cancer, liposomal encapsulation of curcumin and STAT‐3siRNA
significantly inhibited tumor weight and volume progression when
compared with either liposomal curcumin or STAT‐3 siRNA alone.
Consequently, these data suggest that curcumin may inhibit skin cancer
and may provide adjuvant therapy without side effects in skin cancer
The in vivo study on male Wistar rats (Bala et al., 2006) showed that
curcumin can significantly decrease the normal aging‐related factors such
as lipid peroxidation, lipofuscin concentration, and intraneuronal lipofus-
cin accumulation, and enhance the enzymes SOD, GPx, and Na(+), K(+)
adenosine triphosphatase. Curcumin prevents premature aging of skin by
quenching free radicals and reducing inflammation, and has antiproli-
ferative properties through inhibition of NF‐kB, TNF‐α,andMAPK
pathway inhibition, as well as suppression of TGF‐β(Tsai et al., 2012).
Curcumin also partially prevents UV damage that may decrease the
development of skin tumors and be an effective factor for prevention of
premature aging (Bala et al., 2006).
Infectious diseases are a global issue and a wide range of synthetic–
semisynthetic antibiotics have been developed for their treatment.
The development of multidrug resistant bacteria is an evolving health
problem and a major concern; hence, the need for new antibacterial
agents. The major drawbacks of many of these new drugs are their
expense, limited therapeutic window, mode of delivery, rapid
bacterial resistance and their side effects. Minimal or limited side
effects associated with natural products has led to an increasing
research focus to further investigate their use in this scenario.
Curcumin’s antimicrobial effects have been demonstrated in
several studies (Krausz et al., 2015; Luer, Troller, Jetter, Spaniol, &
Aebi, 2011). Krausz et al. (2015) studied the effect of curc‐np as
antimicrobial agents on wound healing. According to this study, curc‐
np exhibited a significant antimicrobial effect against methicillin‐
resistant Staphylococcus aureus strain (MRSA) and Pseudomonas
aeruginosa (97.0% reduction of MRSA growth and 59.2% reduction
of P. aeruginosa growth by colony-forming unit (CFU) quantification)
from 8 hr onwards, in comparison to both untreated control and
control np (p≤0.0001). They showed that curcumin decreases the
bundling of FtsZ protofilaments (which are associated with binding
ability to the cellular proteins FtsZ32 and sortase A). As a result,
cytokinesis and cellular adhesion are interrupted, which also
interferes with the formation of a biofilm. Curcumin’s antibacterial
mechanisms involve suppression of bacterial cell proliferation due to
the inhibition of assembly dynamics of FtsZ (FtsZ polymerization) in
the Z‐ring, which subsequently leads to interruption of prokaryotic
cell division. Also, Tortik, Steinbacher, Maisch, Spaeth, & Plaetzer
(2016) showed that curcumin has high photo killing efficiency against
microorganisms and a high photobleaching effect using a photo-
dynamic inactivation technique. This technique combines a harmless
visible light and a photosensitizer to kill pathogens through ROS
generation. Natural photoactive compounds, like curcumin, are cost‐
effective and provide excellent biocompatibility for most conceivable
applications. Consequently, the photosensitivity of human skin due to
prolonged exposure is decreased. According to several studies, it is
notable that the antibacterial effect of curcumin is greater against
Gram‐positive rather than Gram‐negative species (due to less
interaction with Gram‐negative bacterial cell membranes; Afshariani
et al., 2014; Bhawana, Basniwal, Buttar, Jain, & Jain N., 2011; Krausz
et al., 2015; Luer et al., 2011; Tortik et al., 2016). To increase the
antimicrobial effect of curcumin on Gram‐negative species like
Escherichia coli, Tortik et al. (2016) added calcium chloride to increase
permeability of the Gram‐negative bacterial cell membranes.
Curcumin can also work synergistically with antibiotics (Bhawana
et al., 2011; Mun et al., 2013), such as penicillin, ampicillin, oxacillin,
and norfloxacin, against the MRSA. Curcumin’s poor solubility in
water can be improved by the preparation of polyvinylpyrrolidone‐
curcumin (Tortik et al., 2016), which is efficacious against liquid
cultures of Gram‐positive S. aureus as well as Gram‐negative E. coli
after in vitro permeabilization is enhanced with the inclusion of
. Izui et al. (2016) studied the effect of curcumin against
homotypic and heterotypic biofilm formation. Their results showed
that curcumin prevented Porphyromonas gingivalis OMZ314 homo-
typic biofilm formation and that this effect was dose‐dependent,
inhibition surpassing 70% and 80% using 10 and 20 μg/ml of
curcumin, respectively. The effect of curcumin in preventing the
formation of heterotypic biofilm formation using P. gingivalis
OMZ314 and Streptococcus gordonii G9B showed curcumin’s inhibi-
tion of heterotypic biofilm formation was again dose‐dependent,
curcumin inhibiting biofilm formation by 55%, 80%, and 90% using
5, 10, and 20 μg/ml, respectively. Consequently, the anti‐infective
properties of curcumin make it a promising natural agent for wound
healing, acne treatment and treatment of skin infections.
Acne vulgaris is a long‐term and cutaneous pleomorphic skin
disease of the pilosebaceous unit involving abnormalities in
PANAHI ET AL.
TABLE 1 Studies of curcumin’s effects in dermatological diseasesIn vivo
application Formulation Test model
2 mg/ml curcumin in 0.5%
CMC‐Na (topical) 10 mM for the
treatment of HaCaT cells
Hairless mice and HaCaT
In vivo, in vitro 1–4
days; 24 hr
Curcumin is an active agent for
preventing and treating UV radiation‐
induced acute inflammation and
photoaging due to antioxidant defenses
and inhibition of oxidative damages via
regulating Nrf2 signaling pathway
H. Li et al. (2016)
10–30 μM curcumin Human foreskin (human
In vitro 24 hr Curcumin inhibit the UVB‐induced
expression of MMPs and blocks ROS
production and the MAPK/NF‐jB/AP‐1
signalling pathway in human dermal
fibroblasts (HDFs). Therefore, an
effective therapeutic candidate for
preventing and treating of skin
Phillips et al. (2013)
10 μmol/L curcumin Murine epidermal In vitro 24 hr Prevent UVB‐induced both mTOR and
FGFR2 signaling potentially leading to
a new therapeutic candidate for
advanced cancer with dual pathway
et al. (2016)
25 μM curcumin Melanoma cell culture In vitro 24 hr Curcumin‐induced melanoma cell
death by associated with mPTP
Qiu et al. (2014)
15 mg/100 µl (topical and oral) SKH‐1 hairless mice In vivo ‐Curcumin inhibits UV radiation–
induced skin cancer and prolong time
to tumor onset
Phillips et al. (2013)
0.02% wt/wt (oral) Mouse In vivo 1–14 weeks Curcumin present high
anticarcinogenic activity in skin
cancer through the inhibition of IGF‐1
H. Kim et al. (2014)
5 and 15 mg/day (oral) SCID mice In vivo 24 days Curcumin inhibit skin squamous cell
carcinoma growth and blocks tumor
progression by inhibiting pS6 and
Phillips et al. (2011)
0.1–1.0 mg/ml CCNGs Human melanoma cell,
human dermal fibroblast,
and porcine skin
In vitro 6–24 hr Effective transdermal penetration of
CCNGs could leading to specific
advantage for the treatment of
et al. (2012)
Curcumin nanoniosome gel
(3.15 ± 0.086 drug loading;
Swiss albino mice In vivo 7 weeks Effective transdermal penetration of
curcumin nanoniosome significantly
inhibit proliferation of squamous cell
carcinoma in DMBA‐treated animals
et al. (2015)
PANAHI ET AL.
TABLE 1 (Continued)
application Formulation Test model
Antimicrobial 0.0003–0.0004 g/L curcumin
loaded nanocubosomal hydrogel
Escherichia coli In vitro 24 hr Enhance bioavailability of curcumin
able to increase curcumin
antibacterial activity in topical drug
et al. (2014)
50 or 100 μM curcuminbound to
Staphylococcus aureus,E. coli Ex vivo
24 hr Increase water solubility of curcumin
and highly efficient against S. aureus
an antibacterial against E. coli
Tortik et al. (2016)
5–10 mg/ml curcumin‐
In vitro 24 hr Inhibit growth of Gram‐positive and
Krausz et al. (2015)
100–400 μg/ml curcumin
S. aureus, Bacillus subtilis, E.
coli, P. aeruginosa,
In vitro 24 hr Higher aqueous solubility and more
effective antimicrobial activity of
curcumin nanoparticle compare to
et al. (2011)
7−250 μg/ml curcumin S. aureus In vitro 24 hr Curcumin has synergistic effect in
combination with antibiotics
Mun et al. (2013)
Wound healing 2 g/L curcumin in chloroform
polyvinylpyrrolidone and ethyl
Rat In vivo 21 days A combination of polyvinylpyrrolidone
and ethyl cellulose significantly
improve the permeation of curcumin
transdermal patch leading to
acceleration of wound healing and
Curcumin cream (200 mg per
Breastfeeding women with
Clinical 72 hr Topical application of curcumin
significantly decrease the signs of
lactational mastitis such as pain,
breast tension, and erythema
et al. (2014)
2% concentration curcumin
Rat In vivo 21 days A decrease in size of the burn wounds
and a reduction in inflammation after
et al. (2015)
of curcumin (topical) Mini‐pig In vivo 35 days Reduce expression of cyclooxygenase‐
2 and NF‐kB, and decrease the
epithelial desquamation lead to
stimulation of wound healing
J. Kim et al. (2016)
10 mg/ml quercetin and curcumin‐
loaded phospholipid liposome
Newborn pig skin, mice In vitro, in vivo 1 day,
Increase drug bioavailability and
prevent the formation of skin lesion
et al. (2014)
100 mg/kg body weight (topical) Wistar‐albino rats In vivo 12 days Rise in the hydroxyproline levels and
expression of PCNA in skin
tissuesbytopical application of
curcumin leading much faster wound
et al. (2011)
PANAHI ET AL.
TABLE 1 (Continued)
application Formulation Test model
Encapsulated curcumin loaded in
polymeric micelles in thermo‐
sensitive hydrogel composite
Sprague–Dawley albino rat In vivo 7 days Very good wound healing activity
present in both linear incision and
full‐thickness excision wound model
Krausz et al. (2015)
Curcumin‐loaded hydrogel of
xanthan and galactomannan
Rat In vitro, in vivo 12 hr,
Curcumin loaded into xanthan–
galactomannan hydrogels present
good skin permeation and topical
Koop et al. (2015)
2 g/L of curcumin‐loaded vesicular
Female Laca mice and male
Ex vivo, in vitro 24 hr Improve the skin permeability of
curcumin and bioavailability leading
to significant inflammatory
et al. (2015)
0.145% wt/wt nanocurcumin gel
Wistar rat In vivo 12 days High shelf life and effective anti‐
40 mg/kg curcumin (oral) Mice In vivo 20 days Depress expression of cytokines and
T‐cell proliferation though Kv1.3
channelinhabitation lead to a great
therapeuticeffect without obvious
Kang et al. (2016)
Tablets containing 100 mg of
standardized Curcuma longa
extract with 12 mg of curcumin
per tablet (oral)
Patient male and female Clinical 75 days Combination of the oral curcuma
extract and UVA or visible light
irradiation improve treatment rate of
moderate‐to‐severe plaque psoriasis
et al. (2015)
10 μM of curcumin (oral) Mouse In vivo 20 days Significantly inhibited secretion of
inflammatory factors including
interleukins, TNF‐αin T cells and a
great potential to treat psoriasis
without toxicity to kidney
Kang et al. (2016)
Encapsulation of curcumin in poly
Mice In vivo 7 days Significantly increase curcumin
accumulation, skin penetration and
entrance the blood circulation, which
improves antipsoriasis activity
Sun et al. (2017)
PANAHI ET AL.
sebum production that occurs when hair follicles are clogged with
dead skin cells and oil from the skin. Five important factors in the
pathophysiology of acne generation are (a) excess sebum
secretion from sebaceous glands, (b) bacterial infection (Propio-
nibacterium acnes), (c) follicular epidermal hyperproliferation, (d)
inflammation, and (e) genetics (Beylot et al., 2014; Williams,
Dellavalle, & Garner, 2012). Different gene candidates have been
proposed, including certain variations in TNF‐α,IL‐1α,and
CYP1A1 genes, among others. Acne can create either nonin-
flammatory or inflammatory lesions, mostly affecting the face but
also the back and chest. Although the use of antibiotics is a
currently acceptable method to treat acne, the side effects of
antibiotics and development of antibiotic resistance in Staphylo-
coccus epidermidis demonstrates the need for nontraditional
antimicrobial agents in the treatment of acne vulgaris.
Curcumin’s anti‐inflammatory and antimicrobial properties make
it an ideal candidate for acne treatment. C. H. Liu & Huang (2012)
developed a curcumin‐loaded myristic acid microemulsion which was
shown to be an excellent vehicle for delivering curcumin and
inhibiting S. epidermidis (a bacteria involved in acne). Thus, curcumin
is a promising therapeutic agent for the topical treatment of acne
vulgaris. Also, in other studies by C. H. Liu & Huang (2013)), an
emulsion of curcumin‐loaded lauric acid lipid vehicles showed
antibacterial activity against propionibacteria species (the primary
agent involved in inflammatory acne). The effectiveness of this
emulsion was considerably increased by the nanosized vehicle due to
enhanced effective contact with the bacteria and increased cell
In spite of these numerous advantages, the limitations to the use of
curcumin, which include bioavailability challenges, low stability, low
skin penetration, limited water solubility, and instability following
exposure to light in the UV‐visible range, has meant that this
bioactive compound has found limited use as a pharmaceutical
ingredient (Jafari, Sabahi, & Rahaie, 2016; Liang, Friedman, &
Nacharaju, 2017). Notably, reports (Arunraj et al., 2014) have
shown that curcumin’s antioxidant and anti‐inflammatory proper-
ties are not only decreased following light exposure but, in
addition, it can induce oxidative stress, apoptosis–necrosis, cell
injury, and cell death. In fact, the phototoxic and photosensitizing
effects of crude curcumin are controversial. According to the
literature (Mondal, Ghosh, & Moulik, 2016), the absorption spectra
of curcumin falls in the UV‐visible range, indicating its photo-
degradability. Additionally, poor bioavailability of curcumin (W. Liu
et al., 2016; Prasad, Tyagi, & Aggarwal, 2014) makes it a class II
drug in the biopharmaceutics classification system. In the last
couple of decades, nanotechnology has been used to increase the
stability of drugs, decrease side effects, and improve their delivery
(Arunraj et al., 2014; Rachmawati, Budiputra, & Mauludin, 2015).
Recently, to overcome some of the limitations of curcumin,
TABLE 1 (Continued)
application Formulation Test model
Acne treatment 0.43 µg/ml of Curcumin Pig skin In vitro 24 hr Combined curcumin‐lauric acid in the
nanosized vehicles significantly inhibit
the growth of Propionibacterium acnes
and present a treatment of acne
C. H. Liu and
100 mg/kg curcumin (oral) Mouse In vivo 20 days Significant raise the glutathione
concentration and activities of GPx
and SOD enzymes in skin, whereas
lipid peroxidation declined
significantly meaning to antioxidant
status of Curcumin
Note.AP‐1: activating protein 1; CCNG: curcumin‐loaded chitin‐nanogel; DMBA: 7,12‐Dimethylbenz[a]anthracene; FGFR2: Fibroblast growth factor receptor 2; GPx: glutathione peroxidase; IGF‐1: Insulin‐like
growth factor 1; MAPK: mitogen‐activated protein kinase; mPTP: 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine; mTOR: mammalian target of rapamycin; NF‐kB: nuclear factor κ‐light‐chain‐enhancer of
activated B cells; PCNA: proliferating cell nuclear antigen; ROS: reactive oxygen species; SOD: superoxide dismutase; TNF‐α: tumor necrosis factor α; UVB: ultraviolet B.
PANAHI ET AL.
different curcumin encapsulated formulations on a nanosize
and microsize scale, including liposomes–phospholipid (Manconi
et al., 2017), nanogels (Mangalathillam et al., 2012), mono‐oleine
aqueous dispersion (Puglia et al., 2013), nanostructured lipid
carriers (Chanburee & Tiyaboonchai, 2017), nanoemulsions (Kumar
et al., 2016), polymeric micelles (M. Li et al., 2016) and polymeric
nanoparticles (Yin, Zhang, Wu, Huang, & Chen, 2013), elastic
vesicular systems (R. Agrawal et al., 2015), and lamellar and
hexagonal mesophases (Fonseca‐Santos, Dos Santos, Rodero,
Gremiao, & Chorilli, 2016) have been investigated and have
demonstrated improved aqueous solubility, bioavailability, and
increased targeting potential. Additionally, continuous, low‐level
release of curcumin from encapsulated formulations should protect
encapsulated compounds (including curcumin) from air‐induced
oxidation and may afford long‐term activity and stability. As an
example, Al‐Rohaimi (2015) has shown that the permeation rate,
drug release parameters, shelf‐life, and anti‐inflammatory activity
of curcumin noticeably improved by using amorphous NanoCur as
the source of curcumin, which was then incorporated into a
nanoemulsion (o/w) using a water titration method and subse-
quently evaluated for topical drug delivery. Also, some research
groups (Jeengar, Rompicharla, et al., 2016; Jeengar, Shrivastava,
Mouli Veeravalli, Naidu, & Sistla, 2016) have introduced the use of
emu oil as a carrier for topical curcumin application due to
increased solubility and improved skin penetration, resulting in a
synergistic anti‐inflammatory effect. It should, however, be noted
that the use of emu oil as an anti‐inflammatory agent is
controversial. On the other hand, ethanol, dimethyl sulfoxide, and
propylene glycol were used as solvents for curcumin in aqueous
formulations such as curcumin gels. Menthol has been proposed as
a penetration enhancing agent in preparations of curcumin gels for
topical application due to enhanced percutaneous flux and
transdermal absorption of curcumin (Patel, Patel, & Patel, 2009).
Also, some polymers, such as carbopol, hydroxypropyl methylcel-
lulose, and sodium alginate have been introduced into formulations
to serve as gelling agents and have shown enhanced bioavailability
and dermal permeation of curcumin (Patel et al., 2009).
Curcumin exhibits a variety of important properties and holds
promise for the treatment of dermatological diseases as summarized
in Table 1. Recently, clinical research and preclinical scientific studies
have demonstrated curcumin’s remarkable antioxidant, anti‐inflam-
matory, and antibacterial activities, which can be effectively
utilized to treat acne, psoriasis, dermal wounds, sun burn, premature
aging, melanoma, and ROS agglomeration.
Finally, it would appear that the limitations of poor bioavailability
and low stability of curcumin can be overcome using nanotechnology,
including liposomes–phospholipid, nanogels, nanostructured lipid
carriers, nanoemulsions, polymeric micelles, and various polymeric
nanoparticulate methods, though further studies are needed to
clarify the utility of curcumin.
The authors are thankful to the Clinical Research Development Unit
of the Baqiyatallah Hospital (Tehran, Iran).
CONFLICT OF INTERESTS
Muhammed Majeed is the Founder and Chairman of Sabinsa
Corporation and Sami Labs Limited. For remaining authors, there
are no conflicts of interest.
Stephen L. Atkin http://orcid.org/0000-0002-5887-7257
Amirhossein Sahebkar http://orcid.org/0000-0002-8656-1444
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How to cite this article: Panahi Y, Fazlolahzadeh O, Atkin SL,
et al. Evidence of curcumin and curcumin analogue effects in
skin diseases: A narrative review. J Cell Physiol. 2018;1–14.
PANAHI ET AL.