Article Publish Status: FREE
Abstract Title:

Curcumin ameliorates hepatic fibrosis in type 2 diabetes mellitus-insights into its mechanisms of action.

Abstract Source:

Br J Pharmacol. 2012 Mar 27. Epub 2012 Mar 27. PMID: 22452372

Abstract Author(s):

B Stefanska

Article Affiliation:

Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.


A wide variety of beneficial effects have been attributed to curcumin, a major polyphenol from the golden spice Curcuma longa known as turmeric, including amelioration of severe complications of type 2 diabetes such as hepatic fibrosis, retinopathy, neuropathy, and nephropathy. In the present issue of the BJP, Lin and colleagues reveal new mechanisms by which curcumin inhibits the activation of hepatic stellate cells in vitro, a hallmark of non-alcoholic steatohepatitis and hepatic fibrogenesis associated with type 2 diabetes mellitus. They demonstrate that curcumin suppresses the advanced glycation end-products (AGEs)-mediated induction of the receptor for AGEs (RAGE) gene expression by increasing peroxisome proliferator-activated receptor gamma (PPARG) activity and stimulating de novo synthesis of glutathione. As a result, downstream elements of RAGE activated pathways are inhibited, which prevents oxidative stress, inflammation, and hepatic stellate cell activation. This report suggests that curcumin may have a potential application as an anti-fibrotic agent in type 2 diabetes and opens the door to the evaluation of curcumin therapeutic effects in liver conditions of different aetiology and in other disorders linked to the impairment of PPARG activity, such as obesity and atherosclerosis.© 2012 The Author. British Journal of Pharmacology © 2012 The British Pharmacological Society.

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