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.

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Available from: Young-Sup Lee, Jan 07, 2015
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    • "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). "
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    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.
    Molecular pharmacology 12/2014; 87(3). DOI:10.1124/mol.114.096016 · 4.13 Impact Factor
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    • "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]. "
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    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.
    BioMed Research International 05/2014; 2014:987149. DOI:10.1155/2014/987149 · 1.58 Impact Factor
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    • "Curcumin, a small bioactive molecule derived from a common spice (Turmeric) has been considered as potentially very effective and well-tolerated adjuvant therapy in cancer and inflammation [55], [56]. Among other mechanisms of action, cell cycle arrest, induction of apoptosis, regulation of epigenetic events, inhibition of angiogenesis, chemo- and radio-sensitization, have resulted in many preclinical studies and clinical trials. "
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    ABSTRACT: Cortactin (CTTN), first identified as a major substrate of the Src tyrosine kinase, actively participates in branching F-actin assembly and in cell motility and invasion. CTTN gene is amplified and its protein is overexpressed in several types of cancer. The phosphorylated form of cortactin (pTyr(421)) is required for cancer cell motility and invasion. In this study, we demonstrate that a majority of the tested primary colorectal tumor specimens show greatly enhanced expression of pTyr(421)-CTTN, but no change at the mRNA level as compared to healthy subjects, thus suggesting post-translational activation rather than gene amplification in these tumors. Curcumin (diferulolylmethane), a natural compound with promising chemopreventive and chemosensitizing effects, reduced the indirect association of cortactin with the plasma membrane protein fraction in colon adenocarcinoma cells as measured by surface biotinylation, mass spectrometry, and Western blotting. Curcumin significantly decreased the pTyr(421)-CTTN in HCT116 cells and SW480 cells, but was ineffective in HT-29 cells. Curcumin physically interacted with PTPN1 tyrosine phosphatases to increase its activity and lead to dephosphorylation of pTyr(421)-CTTN. PTPN1 inhibition eliminated the effects of curcumin on pTyr(421)-CTTN. Transduction with adenovirally-encoded CTTN increased migration of HCT116, SW480, and HT-29. Curcumin decreased migration of HCT116 and SW480 cells which highly express PTPN1, but not of HT-29 cells with significantly reduced endogenous expression of PTPN1. Curcumin significantly reduced the physical interaction of CTTN and pTyr(421)-CTTN with p120 catenin (CTNND1). Collectively, these data suggest that curcumin is an activator of PTPN1 and can reduce cell motility in colon cancer via dephosphorylation of pTyr(421)-CTTN which could be exploited for novel therapeutic approaches in colon cancer therapy based on tumor pTyr(421)-CTTN expression.
    PLoS ONE 01/2014; 9(1):e85796. DOI:10.1371/journal.pone.0085796 · 3.23 Impact Factor
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