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ANTI-AGEING NATURAL HERBS: A SYSTEMIC REVIEW

September 2018
Indian Research Journal of Pharmacy and Science 5(3):1589-1598

DOI:10.21276/irjps.2018.5.3.4

Authors:

Saumendu Deb Roy

Mata Gujri College of Pharmacy Mata Gujri University

Mitochondrial damage.

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Turmeric Fig.8: Honey

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Ginseng Fig.10: Liquorice

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Jatamansi Fig.12: Arjuna

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Content uploaded by Saumendu Deb Roy

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Indian Research Journal of Pharmacy and Science; Editorial; A. Chakraborty

et.al

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ANTI-AGEING NATURAL HERBS: A SYSTEMIC REVIEW

Atyurmila Chakraborty*, Mitali Sahoo, Saumendu Deb Roy, Ramesh Kumari Dasgupta

Dept. of Pharmacognosy, Bharat Technology, Uluberia, Howrah

ABSTRACT: Skin is the largest organ of the integumentary system. The overall well-being& perception of health

in humans, very much depends on skin health & beauty. Skin plays a vital role in immunity& protects the body

against pathogens, maintains water and electrolyte balance & also regulates body temperature. Epidermis is the

protective covering over the body surface which serves as a barrier to infection. Thinning of this epidermal layer,

loosening of collagen & elastic fiber, leads to the wrinkle formation and causes ageing. Ageing occurs due to the

intrinsic factors like genetics, cellular metabolism, hormone & metabolic process or extrinsic factors like sun

exposure, smoking, diet and pollution. In this era of modern science, people choose natural herbs rather than plastic

surgery or laser therapy for not only looking younger but also to reduce complications. Herbs help in biological

functioning of the skin & supplies nutrients required for healthy skin. Herbs contain several phytochemicals like

carotenoids, terpenoids, polyphenols which possesses anti-aging activity. A few herb which shows anti-aging

activity includes, Aloe, Cucumber, Ginseng, Honey, Wheat, Liquorice, Arjuna, Jatamansi etc.

KEYWORDS: Herbs, Anti-aging, Skin, Phytochemicals

Corresponding Author: Atyurmila Chakraborty

E-Mail: milachakraborty1996@gmail.com

Phone: +91-8617390669

REVIEW

Submitted on: 12.08.18; Revised on: 19.08.18; Accepted on: 28.08.18

Indian Research Journal of Pharmacy and Science; 17(2018)1589-1598

;

Journal Home Page: https://www.irjps.in

DOI: 10.21276/irjps.2018.5.3.4

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INTRODUCTION:

Ageing is an unavoidable process for all living

organisms. Ageing phenomena starts from the

moment of our birth and is markedly visible on the

skin in progressive years. Based on increased life

expectancy, it is estimated that there will be over 1.2

billion older adults (over 60 years old) worldwide in

2025.

Ageing is at least partially attributed to an age

related increase in weakness and immunosenscence

and perhaps mitochondrial dysfunction.

Maintenance of the physical function in older adults

is therefore a major public and clinical priority. In

humans the skin is the tissue most markedly affected.

Skin is a protective barrier against the external

environment. Its function is to regulate temperature,

fluid balance & to protect from harmful microbes and

UV radiation in sunlight. Two types of skin ageing

exist: age-dependent/chronological ageing and

premature ageing/photoageing. Photoageing is caused

by extrinsic factors and includes signs such as a

leathery appearance, dark/light pigmentation and

deep furrows.

Natural ageing is visible as wrinkling

of the skin. The skin is divided into three layers; the

epidermis, dermis and subcutaneous tissue.

The extracellular matrix (ECM) is the outermost part

of the skin and is composed of fibroblasts and

proteins including collagen and elastin. After the age

of 20, its symptoms appears as the collagen content

per unit area starts decreasing, there is 1% decrease

in collagen content per unit area of the skin every

year. The ECM provides a structural supporting

structure which is essential for growth and elasticity

of the skin and plays an important role in the

maintenance of physiological functions of the body.

Degenaration of the ECM has directly been linked to

skin ageing and is correlated with an increase in

activity of certain enzymes involved in skin ageing,

which includes hyaluronidase, elastase and

collagenase. Collagen is one of the major building

blocks of the skin, which is responsible for the

elasticity and strength of the skin and maintains its

flexibility. Hyaluronic acid performs a role in

retaining the moisture of the skin, as well as its

structure and elasticity. It also facilitates the

exchange of nutrients and waste products and is

participating in rapid tissue proliferation,

regeneration and repair. With ageing, collagen,

elastin and hyaluronic acid levels declines, leading to

a loss of strength and flexibility in the skin which

results in visible wrinkles associated with the

thickened epidermis, mottled discoloration, laxity,

dullness and roughness of the skin.

Reactive oxygen species (ROS) play an important

role in many cellular mechanism . When UV

radiation is absorbed by the skin, it leads to enhanced

ROS generation and induction of oxidative stress.

Oxidative damage may lead to lipid peroxide

formation, mitochondrial and DNA damage, and

protein and gene modification which change protein

structure and function. High levels of ROS lead to the

activation of hyaluronidase, collagenase and elastase,

which can further contribute to skin ageing.

The enzyme angiotensin 2 also plays a vital role in

photoaging of skin as it involved in healing wounds

and scar formation, appearance of scars leads to

wrinkles. So by using angiotensin converting enzyme

(ACE) inhibitors which prevent the conversion of

angiotensinogen (inactive) to angiotensin (active) we

can decrease the effect of angiotensin 2 induced skin

ageing and wrinkles.

The modern science and technology provides plastic

surgery, laser rejuvenation, and many more invasive

techniques. Noninvasive techniques do not involve

any risks or complications and mostly free of side

Indian Research Journal of Pharmacy and Science; Editorial; A. Chakraborty

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effects as compared to the invasive techniques which

are more painful and laborious. Over the last decade,

there has been an increase in the use of herbal

extracts in cosmetics to reduce the ageing process.

The extracts of Aloe Vera, Amla, Turmeric,

Cucumber, Ginseng, Honey, Wheat, Liquorice,

Arjuna, Jatamansi are extensively used in herbal

cosmetic industries due to their skin beneficial

properties.

MECHANISM OF SKIN AGING

Extrinsic skin ageing:-

This is caused by environmental factors, such as

exposure to the sun rays, repetitive facial expressions,

gravity, sleeping positions and smoking.

Extrinsic

ageing is caused by chronic exposure to UV light, so

it is also known as photoageing.

Extrinsic skin

ageing is a collective process and depends mostly on

the degree of sun exposure and skin pigment. With

chronic skin exposure to UV rays, the stratum

corneum layer of skin thickens, the epidermis is

damaged and there is progressive dysplasia with

cellular atypia and anaplasia, reduction in collagen

and degradation of elastic fibres.

a. Membrane/ nuclear signaling:-

UV irradiation provokes reactive

oxygen species (ROS) which repress the

activity of enzyme protein tyrosine

phosphatase κ. This enzyme maintains

cell surface receptors of skin, including

receptors for epidermal growth

factor(EGF), interleukin (IL)-1,

keratinocyte growth factor and tumour

necrosis factor (TNF)-α in an inactive

(hypophosphorylated) state.

Activated

receptors impel to intracellular

signaling through stimulation of the

stress-associated mitrogen activated

protein (MAP) kinases p38 and c-Jun

amino terminal kinase (JNK). Kinase

activation induces the transcription of

MMPs (matrix metalloproteinase) and

decreases expression of the procollagen

I and III and TGF-β receptors, with

afinal outcome of reduced dermal

matrix formation and hence, it reduces

the synthesis of collagen.

Fig.1: Nuclear Signaling

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b. Mitochondrial damage :-

Mitochondria are cellular organelles

that generate energy (ATP) by

compelling oxygen. UV effect on the

mitochondria electron transport chain

produces abundant ROS that can

damage mitochondrial DNA

(mtDNA).The mitochondrial genome

encodes 13 components of the electron

transport chain and oxidative damage

may be foremost to deletions or

rearrangements of the DNA, most likely

due to double-strand breaks which may

affect mitochondrial ability to generate

energy for the cell. It is inferred that the

consequent decrease in mitochondrial

function photodamaged skin leads to

additional accumulation of ROS and

further compromises the cell’s ability to

initiate energy.

Fig. 2: Mitochondrial damage.

c. Protein oxidation :-

Oxidative damage can also affect

proteins and photodamaged skin.

Oxidative protein impair may result in

loss or gain of activity (i.e. enzymes),

loss of structural protein function and

increased/decreased susceptibility to

degradation.

d. Telomere :-

Telomeres are tandem repeats of a short

sequence TTAGGG. It exists in a loop

configuration. Telomeres become

critically short when these loop is

disrupted by cell division or UV

irradiation. During cell division

telomeres cap (the terminal portion of

chromosomes, preventing the fusion of

telomeres with each other) cannot be

replicated, so the bases of the telomeres

caps are lost with each cell division and

finally enters a state of senescence or

apoptosis. When telomeres are damaged

by UV irradiation the loops

configuration becomes disclosed and

through interaction with the protein

activates the tumour suppressor protein

p53 and other proteins which

responsible for DNA damage and also

induces senescence or apoptosis.

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Fig.3: Telomerase induced skin aging

Intrinsic skin ageing: -

Intrinsic skin ageing, also known as natural ageing

mostly found in sun protected area. It is due to the

passage of time or by the inherited gene, therefore

also termed as chronological ageing. Basically the

molecular machanisms of both the type of skin

ageing (extrinsic and intrinsic) are similar, for

example shortening of telomeres, mutations of

mitochondrial DNA, oxidative stress, genetic

mutations and decrease of many hormone levels.

According to the free radical theory of ageing, ROS,

chiefly commencing from oxidative cell metabolism,

play a notable role in both chronological ageing and

photoageing. ROS influence the transcription factor

c-Jun via MAPK (mitrogen activated protein

kinase).Intrinsic skin ageing as same like extrinsic

ageing and collagen is degraded present in

intrinsically aged skin similar to photoaged skin.

Hormonal changes can also alter intrinsic skin

ageing. The exhibition of sex hormones in the

gonads, the pituitary and adrenal glands already

gradually decline in the mid-twenties. The hormone

oestrogen and progesterone start decreasing during

menopause. In particular, the imperfection in

oestrogens and androgens cause dryness, wrinkling,

epidermal atrophy, collagen breakdown and loss of

elasticity.

NATURAL HERBS USED FOR ANTI-

AGEING:-

Herbal cosmetics play a leading role in impeding and

reversing ageing of skin. Ingredients present in herbal

cosmetics impact biological functions of skin and it

also provide required nutrition for healthy skin. It

has been estimated that more than 50% of all the

drugs in the world are natural products and their

derivatives, and plant-based health remedies are

promising. The application of herbal anti ageing

products has been proliferated to many folds in

personal care practices. The recent trends in anti-

ageing skin care products is focussed on developing

new plant extracts and botanical ingredients based on

their traditional medicinal uses which leads to the

emergence of several cosmoceuticals that prevent

wrinkles and protect the skin from any kind of

unwanted symptoms.

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NA TURAL ANTI_AGING HERBS

14 , 15 , 16

 AL OE V ERA

Biological Source: Aloes are the dried juice of

leaves of Aloe barbadensis, belonging to the family

Liliaceae.

Phyto-constituents: All the varieties of aloe are the

major sources of anthraquinone glycosides. The

principal active constituent of aloe is aloin, which is a

mixture of glycosides, among which barbaloin is the

chief constituent. Along with barbaloin, the drug also

contains isobarbaloin, β- barbaloin, aloe-emodin and

resins.

Ro le i n Anti-ageing:

The leaves of aloes are commonly used in anti-aging

and anti-wrinkle creams and moisturizers. In the

treatment of aging and wrinkles the constituents of

aloe Vera such as aloin A and B have shown the

property to inhibit the activity of collagenase, the

enzyme which causes degradation of collagen fibres.

Fig.5: Aloe Fig.6: Amla

Fig. 4: Mechanism of action of Herbs in Anti-a

geing

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 AMLA

Biological Source: This consists of dried as well as

fresh fruits of the plant Emblica officinalis belonging

to the family Euphorbiaceae.

Phyto-constituents: Amla fruit is a natural source of

vitamin C (Ascorbic acid) and also contains fat,

phyllembelin and tannins. Amla fruit is also rich in

mineral matters like phosphorus, iron and calcium.

Role in anti-ageing:

Amla, being a rich source of vitamin C, is considered

important to slow ageing process. It improves skin

health. Ageing is a cumulative result of damage to

various cells and tissues, mainly by oxygen free

radicals. Vitamin C is a scavenger of free radicals

which breaks them down.

 TURMERIC

Biological Source: Turmeric consists of dried as well

as, fresh rhizomes of the plant Curcuma longa

belonging to the family Zingiberaceae.

Phyto-constituents: Turmeric contains a yellow

coloured substance known as curcuminoids. The

chief component of curcuminoids is known as

curcumin (50-60%). It also contains volatile oil,

resin, camphor, camphene etc.

Role in anti-ageing:

The chief constituent of Turmeric is curcumin which

acts as a superoxide scavenger & as a singlet oxygen

quencher. Therefore, the anti-ageing property of

Turmeric is mainly due to the curcumin.

Fig.7: Turmeric Fig.8: Honey

 HONEY

Biological Source: Honey is a sugar secretion

deposited in honey comb by the bees, Apis mellifera

and other species of Apis, belonging to the family

Apidae.

.Phyto-constituents: Honey is an aqueous solution

of glucose (35%), fructose (45%) and sucrose (2%).It

also contains maltose, gum, polyphenols, flavonoids,

vitamins, proteins etc.

Role in anti-ageing:

The antioxidant property of Honey is due to the

phenolic compounds (benzoic acid and cinnamic

acid) and flavonoids present in it, which helps to

prevent wrinkles in our skin.

 GINSENG

Biological Source: Ginseng is the dried root of

various species of Panax, like P. ginseng (Korean

ginseng), P. japonica (Japanese ginseng), P.

notoginseng (Chinese ginseng), belonging to the

family Araliaceae.

Phyto-constituents: Ginseng contains a mixture of

several saponin glycosides, belonging to triterpinoid

group. These are Ginsenosides, Panaxosides and

Chikusetsusaponin which are responsible for various

activity of ginseng.

Role in anti-ageing:

The chief constituent of Ginseng is Ginsenoside

which is responsible for the anti ageing activity of the

ginseng. It improves the blood circulation and skin

tone and also moisturizes the skin.

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Fig.9: Ginseng Fig.10: Liquorice

 LIQUORICE

Biological Source: Liquorice consists of dried,

unpeeled, roots and stolons of Glycyrrhiza glabra,

belonging to the family Leguminosae.

Phyto-constituents: The chief constituent is of

liquorice is a triterpenoid saponin known as

glycyrrhizin ( glycyrrhizic acid),which is a potassium

and calcium salt of glycyrrhizinic acid. It also

contains flavonoids, liquiritin and isoliquiritin.

Role in anti-ageing:

The anti ageing activity of liquorice is due to the

presence of phenylflavonoids (dehydroglyasperin C,

dehydroglyasperin D and isoangustone A, which are

acts as superoxide scavenger and prevent wrinkles.

 JATAMANSI

Biological Source: Jatamansi consists of dried

rhizomes of Nardostachys jatamansi belonging to the

family Valerianaceae.

.Phyto-constituents: It contains volatile oil, resin,

sugar, starch and also contains jatamansic acid and

ketones, jatamansone and nardostachnone.

Role in anti-ageing:

Jatamansi triggers fibroblasts to increase the

synthesis of collagen and elastin fibres, due to which

skin elasticity increases and wrinkles formation

(ageing) decreases.

Fig.11: Jatamansi Fig.12: Arjuna

 ARJUNA

Biological Source: Arjuna consists of dried stem

bark of the plant known as Terminalia arjuna,

belonging to the family Combretaceae.

.Phyto-constituents: Arjuna contains tannins,

triterpenoid saponins, arjunolic acid, arjunic acid,

arjungenin. It also contains ellagic acid, arjunine,

arjunolone.

Role in anti-ageing:

Aging occurs due to decrease in the collagen

production. Collagen synthesis and epidermal barrier

function is improved by pentacyclic triterpenoids

found in Terminalia arjuna. It also increases skin

moisturization and decreased scaliness. It strengthens

the skin barrier and induces sebum production to

reduce the signs of dry skin and protect the skin from

external challenges. It also contributes to an

improved blood circulation for better nutrient supply.

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DI SCUSSION:

Phytochemicals derived from plants have a lot of skin

beneficial properties related to UV protection,

antioxidant action, matrix protection and skin

hydration. Over the past decade, a lot of

phytochemicals from the plant extracts have been

explored and their biological activities well-studied

in vitro. Therefore, there is a continuous requirement

for more clinical studies with emphasis on the

concentration of the ingredient in herbal products,

their formulation, safety, and the anti-ageing effect

duration.

ACKNOWLEDGEMENT:

The authors are very much thankful to the

Management of Bharat Technology for providing the

necessary facilities to carry out the study.

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Jan 2016
PLOS ONE

Human skin is body's vital organ constantly exposed to abiotic oxidative stress. This can have deleterious effects on skin such as darkening, skin damage, and aging. Plant-derived products having skin-protective effects are well-known traditionally. Triphala, a formulation of three fruit products, is one of the most important rasayana drugs used in Ayurveda. Several skin care products based on Triphala are available that claim its protective effects on facial skin. However, the skin protective effects of Triphala extract (TE) and its mechanistic action on skin cells have not been elucidated in vitro. Gallic acid, ellagic acid, and chebulinic acid were deduced by LC-MS as the major constituents of TE. The identified key compounds were docked with skin-related proteins to predict their binding affinity. The IC50 values for TE on human dermal fibroblasts (HDF) and human keratinocytes (HaCaT) were 204.90 ± 7.6 and 239.13 ± 4.3 μg/mL respectively. The antioxidant capacity of TE was 481.33 ± 1.5 mM Trolox equivalents in HaCaT cells. Triphala extract inhibited hydrogen peroxide (H2O2) induced RBC haemolysis (IC50 64.95 μg/mL), nitric oxide production by 48.62 ± 2.2%, and showed high reducing power activity. TE also rescued HDF from H2O2-induced damage; inhibited H2O2 induced cellular senescence and protected HDF from DNA damage. TE increased collagen-I, involucrin and filaggrin synthesis by 70.72 ± 2.3%, 67.61 ± 2.1% and 51.91 ± 3.5% in HDF or HaCaT cells respectively. TE also exhibited anti-tyrosinase and melanin inhibition properties in a dose-dependent manner. TE increased the mRNA expression of collagen-I, elastin, superoxide dismutase (SOD-2), aquaporin-3 (AQP-3), filaggrin, involucrin, transglutaminase in HDF or HaCaT cells, and decreased the mRNA levels of tyrosinase in B16F10 cells. Thus, Triphala exhibits protective benefits on skin cells in vitro and can be used as a potential ingredient in skin care formulations.

Mitochondrial Dysfunction during Brain Aging: Role of Oxidative Stress and Modulation by Antioxidant Supplementation

Article

Full-text available

Jun 2011

Mitochondrial dysfunction and oxidative stress are two interdependent and reinforcing damage mechanisms that play a central role in brain aging. Oxidative stress initiated and propagated by active oxyradicals and various other free radicals in the presence of catalytic metal ions not only can damage the phospholipid, protein and DNA molecules within the cell but can also modulate cell signalling pathways and gene expression pattern and all these processes may be of critical importance in the aging of brain. The present article describes the mechanism of formation of reactive oxyradicals within mitochondria and then explains how these can initiate mitochondrial biogenesis program and activate various transcriptional factors in the cytosol to boost up the antioxidative capacity of the mitochondria and the cell. However, a high level of oxidative stress finally inflicts critical damage to the oxidative phosphorylation machinery and mitochondrial DNA (mtDNA). The latter part of the article is a catalogue showing the accumulating evidence in favour of oxidative inactivation of mitochondrial functions in aged brain and the detailed reports of various studies with antioxidant supplementation claiming variable success in preventing the age-related brain mitochondrial decay and cognitive decline. The antioxidant supplementation approach may be of potential help in the management of neurodegenerative diseases like Alzheimer's disease. The newly developed mitochondria-targeted antioxidants have brought a new direction to experimental studies related to oxidative damage and they may provide potential drugs in near future for a variety of diseases or degenerative conditions including brain aging and neurodegenerative disorders.

Mitotic recombination in Saccharomyces cerevisiae

Article

Full-text available

Feb 2003

Mitotic homologous recombination (HR) is an important mechanism for the repair of double-strand breakS and errors occurring during DNA replication. It is likely that the recombinational repair of DNA lesions occurs preferentially by sister chromatid exchanges that have no genetic consequences. However, most genetically detectable HR events occur between homologous DNA sequences located at allelic positions in homologous chromosomes, or between DNA repeats located at ectopic positions in either the same, homologous or heterologous chromosomes. Mitotic recombination may occur by multiple mechanisms, including double-strand break repair, synthesis-dependent strand annealing, break-induced replication and single-strand annealing. The occurrence of one recombination mechanism versus another depends on different elements, including the position of the homologous partner, the initiation event, the length of homology of the recombinant molecules and the genotype. The genetics and molecular biology of the yeast Saccharomyces cerevisiae have proved essential for the understanding of mitotic recombination mechanisms in eukaryotes. Here, we review recent genetic yeast data that contribute to our understanding of the different mechanisms of mitotic recombination and the in vivo role of the recombination proteins.

Inhibition of matrix metalloproteinase-1 activity by the soybean Bowman-Birk inhibitor

Article

Full-text available

Jul 2004

Inductively coupled plasma analysis of soybean Bowman-Birk inhibitor (BBI) indicated that BBI was a metalloprotein which contained magnesium, calcium, and zinc at 0.40, 0.43 and 0.008 atom/mol BBI, respectively. Heparin-enhanced gelatin zymography, quenched fluorescence substrate hydrolysis analysis, and the Biotrak assay of the interaction of BBI with the matrix metalloproteinase-1 (MMP-1) demonstrated that demineralized BBI at 30 nM inhibited MMP-1 activity whereas mineralized BBI was inhibitory at 115 nM.

Oxidative Inhibition of Receptor-type Protein-tyrosine Phosphatase by Ultraviolet Irradiation Activates Epidermal Growth Factor Receptor in Human Keratinocytes

Article

Full-text available

Oct 2006

Ultraviolet (UV) irradiation rapidly increases tyrosine phosphorylation (i.e. activates) of epidermal growth factor receptors (EGFR) in human skin. EGFR-dependent signaling pathways drive increased expression of matrix metalloproteinases, whose actions fragment collagen and elastin fibers, the primary structural protein components in skin connective tissue. Connective tissue fragmentation, which results from chronic exposure to solar UV irradiation, is a major determinant of premature skin aging (photoaging). UV irradiation generates reactive oxygen species, which readily react with conserved cysteine residues in the active site of protein-tyrosine phosphatases (PTP). We report here that EGFR activation by UV irradiation results from oxidative inhibition of receptor type PTP-κ (RPTP-κ). RPTP-κ directly counters intrinsic EGFR tyrosine kinase activity, thereby maintaining EGFR in an inactive state. Reversible, oxidative inactivation of RPTP-κ activity by UV irradiation shifts the kinase-phosphatase balance in favor of EGFR activation. These data delineate a novel mechanism of EGFR regulation and identify RPTP-κ as a key molecular target for antioxidant protection against skin aging.

Chronological and photoaging of the human sebaceous gland

Article

Jan 2001

The human sebaceous gland underlies both extrinsic and intrinsic ageing. The latter is associated with morphological changes and alteration in the sebaceous gland activity. The high androgen-dependent sebum secretion in neonates falls during childhood, starts to rise again during puberty and reaches its maximum in young adults. While the number of sebaceous glands remain the same during life, sebum levels tend to decrease after menopause in females, whereas no major changes appear until the 8th decade of life in men. Reduced androgen levels in aged individuals lead to a slow cellular turnover in the sebaceous glands resulting in hyperplasia of the facial sebaceous glands in advanced age. Ultraviolet radiation and immune suppression (cyclosporine A w/o corticosteroids) represent co-factors for the development of sebaceous gland hyperplasia. Current molecular findings indicate that overexpression of the ageing associated genes Smad7 and parathormone-related protein correlate with sebaceous gland hyperplasia, whereas c-myc overexpression is associated with enhanced sebum production. On the other hand, down-regulation of the mismatch repair genes hMLH-1 and hMSH-2 may promote the development of sebaceous gland carcinoma. In addition to spontaneous single tumors, sebaceous gland carcinomas have been reported in immune-suppressed transplant recipients (azathiorpine, cisplatin, cyclosporine A) and in association with the Muir-Torre syndrome. Microsatellite instability with a loss of the mismatch repair gene hMSH-2 has been detected in immune-suppressed patients and under photo-induced DNA damage. Topical and systemic estrogens offer a treatment options for skin xerosis in menopausal females. A combination of isotretinoin and interferon-alpha seems to prevent tumor development in patients with Muir-Torre syndrome.

Protein oxidative damage

Article

Feb 2000
METHOD ENZYMOL

Emily Shacter

Age-dependent increase of elastase type protease activity in mouse skin. Effect of UV irradiation

Article

Oct 2000
J PHOTOCH PHOTOBIO B

The effect of chronological aging and photoaging (UV-radiation) on elastase-type enzyme activity of hairless mouse skin was studied. Aging resulted in the increase of elastase type endopeptidase activity extractable from mouse skins. Both chronic UVA and UVB radiation resulted in a significant increase of elastase type activity. PBS extracted only small part of the elastase activity, UV-A produced an increase of about 90-120% according to the type of irradiation (xenon or UV-A SUN) and UV-B produced a 72% increase. Extraction by Triton X-100 suggested that most of the activity is bound to cells and fibrous structures. EDTA inhibited 80-90% of the elastase activity in chronologically aged skin extracts and also the activity induced by UVA radiation suggesting that metallo-elastase(s) are involved. About 30% of the UVB induced activity could only be inhibited by EDTA and about 50% by PMSF suggesting that irradiation by UVB increased more serine endopeptidase activity but also MMP-activity. Chronic UVA radiation produced an increase of skin elastase activity equivalent to that observed after 24 months of aging in non-irradiated animals (approximately 100 weeks) corresponding to approximately 90% of total life span of these mice. The total increase produced by UVB was less, but the strong increase of a serine elastase, presumably from PMN-s, appear to produce a much more pronounced biological activity as shown by the presence of fibronectin degradation products in skin extracts. Such degradation products were shown to exert harmful effects on tissues. These results may well have biological significance and distinguish chronological aging and photoaging.

Mechanisms of Photoaging and Chronological Skin Aging

Article

Dec 2002
ARCH DERMATOL

Human skin, like all other organs, undergoes chronological aging. In addition, unlike other organs, skin is in direct contact with the environment and therefore undergoes aging as a consequence of environmental damage. The primary environmental factor that causes human skin aging is UV irradiation from the sun. This sun-induced skin aging (photoaging), like chronological aging, is a cumulative process. However, unlike chronological aging, which depends on the passage of time per se, photoaging depends primarily on the degree of sun exposure and skin pigment. Individuals who have outdoor lifestyles, live in sunny climates, and are lightly pigmented will experience the greatest degree of photoaging. During the last decade, substantial progress has been made in understanding cellular and molecular mechanisms that bring about chronological aging and photoaging. This emerging information reveals that chronological aging and photoaging share fundamental molecular pathways. These new insights regarding convergence of the molecular basis of chronological aging and photoaging provide exciting new opportunities for the development of new anti-aging therapies. This article reviews our current understanding and presents new data about the molecular pathways that mediate skin damage by UV irradiation and by the passage of time.

Photoageing: Mechanism, prevention and therapy

Article

Dec 2007

Photoageing is the superposition of chronic ultraviolet (UV)-induced damage on intrinsic ageing and accounts for most age-associated changes in skin appearance. It is triggered by receptor-initiated signalling, mitochondrial damage, protein oxidation and telomere-based DNA damage responses. Photodamaged skin displays variable epidermal thickness, dermal elastosis, decreased/fragmented collagen, increased matrix-degrading metalloproteinases, inflammatory infiltrates and vessel ectasia. The development of cosmetically pleasing sunscreens that protect against both UVA and UVB irradiation as well as products such as tretinoin that antagonize the UV signalling pathways leading to photoageing are major steps forward in preventing and reversing photoageing. Improved understanding of the skin's innate UV protective mechanisms has also given rise to several novel treatment concepts that promise to revolutionize this field within the coming decade. Such advances should not only allow for the improved appearance of skin in middle age and beyond, but also greatly reduce the accompanying burden of skin cancer.