Curcumin prevents liver fibrosis. - GreenMedInfo Summary

Abstract Title:

Curcumin prevents liver fibrosis by inducing apoptosis and suppressing activation of hepatic stellate cells.

Abstract Source:

J Nat Med. 2009 Oct;63(4):415-20. Epub 2009 Jun 25. PMID: 19554395

Abstract Author(s):

Jian-Chang Shu, Ya-Jun He, Xia Lv, Guo-Rong Ye, Le-Xin Wang

Article Affiliation:

Guangzhou Red Cross Hospital Affiliated to Jinan University Medical College, 510220 Guangzhou, China.


This study was designed to investigate the prophylactic effects and the mechanisms of curcumin on liver fibrosis in rats. Liver fibrosis was induced in 72 Sprague Dawley rats by intraperitoneal injection of carbon tetrachloride. Rats were divided into control, liver fibrosis, high, medium, and low dose curcumin (200, 100, and 50 mg kg(-1), respectively), and colchicine (0.1 mg kg(-1)) groups. After 8 weeks of treatment, histopathological examination was performed on hepatic tissues, and liver fibrosis was graded. Hepatic stellate cells activity was examined by smooth muscle alpha-actin immunohistochemistry staining, and apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling. The liver fibrosis score in the high, medium, and low dose curcumin group (5.79 +/- 1.80, 8.58 +/- 3.34, and 9.58 +/- 3.32, respectively) and the colchicine group (4.91 +/- 1.28) was significantly lower than in the fibrosis group (20.40 +/- 3.38, P<0.01). The ratio of activated hepatic stellate cells in the three curcumin groups (0.97 +/- 0.69, 2.06 +/- 0.58, and 3.49 +/- 1.03, respectively) and the colchicine group (0.78 +/- 0.31) was significantly lower than in the fibrosis group (6.08 +/- 1.13, P<0.05). The apoptosis index in the three curcumin groups (0.57 +/- 0.21, 0.37 +/- 0.22, and 0.34 +/- 0.21, respectively) was higher than in the fibrosis (0.09 +/- 0.09, P<0.05) or the colchicine group (0.16 +/- 0.19, P<0.05). Curcumin prevents carbon tetrachloride-induced liver fibrosis in rats. The prevention of liver fibrosis may be due to the inhibition of the activation of hepatic stellate cells and induction of their apoptosis.

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