Curcumin in inflammatory diseases

School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 702-701, Korea.
BioFactors (Impact Factor: 4.59). 02/2013; 39(1). DOI: 10.1002/biof.1066
Source: PubMed


Curcumin (diferuloylmethane), a yellow coloring agent extracted from turmeric is also used as a remedy for the treatment and prevention of inflammatory diseases. Acute and chronic inflammation is a major factor in the progression of obesity, type II diabetes, arthritis, pancreatitis, cardiovascular, neurodegenerative and metabolic diseases, as well as certain types of cancer. Turmeric has a long history of use in Ayurvedic medicine for the treatment of inflammatory disorders. Recent studies on the efficacy and therapeutic applicability of turmeric have suggested that the active ingredient of tumeric is curcumin. Further, compelling evidence has shown that curcumin has the ability to inhibit inflammatory cell proliferation, invasion, and angiogenesis through multiple molecular targets and mechanisms of action. Curcumin is safe, non-toxic, and mediates its anti-inflammatory effects through the down-regulation of inflammatory transcription factors, cytokines, redox status, protein kinases, and enzymes that all promote inflammation. In addition, curcumin induces apoptosis through mitochondrial and receptor-mediated pathways, as well as activation of caspase cascades. In the current study, the anti-inflammatory effects of curcumin were evaluated relative to various chronic inflammatory diseases. Based on the available pharmacological data obtained from in vitro and in vivo research, as well as clinical trials, an opportunity exists to translate curcumin into clinics for the prevention of inflammatory diseases in the near future. © 2012 BioFactors, 2013.

Download full-text


Available from: Young-Sup Lee, Jan 07, 2015
  • Source
    • "Bcl-2 has become as a target for many years after its widespread expression has observed in breast cancer cells [3]. Curcumin is an effective anticancer compound, which is also commonly used as anti-inflammatory and/or anti-oxidant agent in the treatment of several disease models [4] [5]. Recent studies have shown that curcumin can induce apoptosis via decreasing the expression of Bcl-2 protein in breast cancer cells [6] [7]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Bcl-2 protein has been contributed with number of genes which are involved in oncogenesis. Among the many targets of Bcl-2, NFκB have potential role in induction of cell cycle arrest. Curcumin has potential therapeutic effects against breast cancer through multiple signaling pathways. In this study, we investigated the role of curcumin in induction of cell cycle arrest via regulating of NFκB and polyamine biosynthesis in wt and Bcl-2+ MCF-7 cells. To examine the effect of curcumin on cell cycle regulatory proteins, PI3K/Akt, NFκB pathways and polyamine catabolism, we performed immunoblotting assay. In addition, cell cycle analysis was performed by flow cytometry. The results indicated that curcumin induced cell cycle arrest at G2/M phase by downregulation of cyclin B1 and Cdc2 and inhibited colony formation in MCF-7 wt cells. However, Bcl-2 overexpression prevented the inhibition of cell cycle associated proteins after curcumin treatment. The combination of LY294002, PI3K inhibitor, and curcumin induced cell cycle arrest by decreasing CDK4, CDK2 and cyclin E2 in Bcl-2+ MCF-7 cells. Moreover, LY294002 further inhibited the phosphorylation of Akt in Bcl-2+ MCF-7 cells. Curcumin could suppress the nuclear transport of NFκB through decreasing the interaction of P-IκB-NFκB. The combination of wedelolactone, NFκB inhibitor, and curcumin acted different on SSAT expression in wt MCF-7 and Bcl-2+ MCF-7 cells. NFκB inhibition increased the SSAT after curcumin treatment in Bcl-2 overexpressed MCF-7 cells. Inhibition of NFκB activity as well as suppression of ROS generation with NAC resulted in the partial relief of cells from G2/M checkpoint after curcumin treatment in wt MCF-7 cells. In conclusion, the potential role of curcumin in induction of cell cycle arrest is related with NFκB-regulated polyamine biosynthesis.
    Full-text · Article · Feb 2016 · Biomedecine [?] Pharmacotherapy
  • Source
    • "It has been long known that curcumin has beneficial effects for some conditions and ailments due to now well documented anti-inflammatory effects (Shehzad et al., 2013). Anticarcinogenic, antiangiogenesis, and antimetastatic effects of this natural polyphenol by a plethora of proposed mechanisms have also been described (Kuttan et al., 2007; Fan et al., 2013; Norris et al., 2013). "
    [Show abstract] [Hide abstract]
    ABSTRACT: We have previously reported that curcumin analogs with a C7 linker bearing a C4-C5 olefinic linker with a single keto group at C3 (enone linker) display mid-nanomolar activity against the bloodstream form of Trypanosoma brucei. However, no clear indication of their mechanism of action, or of their superior antiparasitic activity relative to analogs with the original di-ketone curcumin linker, was apparent. In order to further investigate their utility as antiparasitic agents, we here compare the cellular effects of curcumin and the enone linker lead compound, AS-HK014. An AS-HK014-resitant line, TA014, was developed by in vitro exposure to the drug. Metabolomic analysis revealed that exposure to AS-HK014, but not curcumin, rapidly depleted glutathione and trypanothione in the wild-type line, although almost all other metabolites were unchanged relative to control. In TA014 cells thiol levels were similar to untreated wild-type cells, and were not significantly depleted by AS-HK014. Adducts of AS-HK014 with both glutathione and trypanothione were identified in AS-HK014-exposed wild-type cells, and reproduced by chemical reaction. However, adduct accumulation in sensitive cells was much lower than in resistant cells. TA014 cells did not exhibit any changes in sequence or protein levels of glutathione synthetase and γ-glutamylcysteine synthetase relative to wild-type cells. We conclude that mono-enone curcuminoids have a different mode of action than curcumin, rapidly and specifically depleting thiol levels in trypanosomes by forming an adduct. This adduct may ultimately be responsible for the highly potent trypanocidal activity antiparasitic activity of the mono-enone curcuminoids. The American Society for Pharmacology and Experimental Therapeutics.
    Full-text · Article · Dec 2014 · Molecular pharmacology
  • Source
    • "Shehzad et al. described the main roles that curcumin may perform in inflammatory pathways (the most important of them are summarized in Table 1) and in the management of the related chronic inflammatory diseases [85]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Urothelium, in addition to its primary function of barrier, is now understood to act as a complex system of cell communication that exhibits specialized sensory properties in the regulation of physiological or pathological stimuli. Furthermore, it has been hypothesized that bladder inflammation and neoplastic cell growth, the two most representative pathological conditions of the lower urinary tract, may arise from a primary defective urothelial lining. Transient receptor potential vanilloid channel 1 (TRPV1), a receptor widely distributed in lower urinary tract structures and involved in the physiological micturition reflex, was described to have a pathophysiological role in inflammatory conditions and in the genesis and development of urothelial cancer. In our opinion new compounds, such as curcumin, the major component of turmeric Curcuma longa, reported to potentiate the effects of the chemotherapeutic agents used in the management of recurrent urothelial cancer in vitro and also identified as one of several compounds to own the vanillyl structure required to work like a TRPV1 agonist, could be thought as complementary in the clinical management of both the recurrences and the inflammatory effects caused by the endoscopic resection or intravesical chemotherapy administration or could be combined with adjuvant agents to potentiate their antitumoral effect.
    Full-text · Article · May 2014 · BioMed Research International
Show more