Published online May 7, 2015. doi: 10.3748/wjg.v21.i17.5271
Peer-review started: October 29, 2014
First decision: December 26, 2014
Revised: January 27, 2015
Accepted: February 11, 2015
Article in press: February 11, 2015
Published online: May 7, 2015
Processing time: 196 Days and 3.7 Hours
AIM: To investigate anti-apoptotic effects of glycyrrhizic acid (GA) against fibrosis in carbon tetrachloride (CCl4)-induced liver injury and its contributing factors.
METHODS: Liver fibrosis was induced by administration of CCl4 for 8 wk. Pathological changes in the liver of rats were examined by hematoxylin-eosin staining. Collagen fibers were detected by Sirius red staining. Hepatocyte apoptosis was determined by TUNEL assay and the expression levels of cleaved caspase-3, Bax, α-SMA, connective tissue growth factor (CTGF), matrix metalloproteinase (MMP) 2 and MMP9 proteins were evaluated by western blot analysis, and α-SMA mRNA, collagen type I and III mRNA were estimated by real-time PCR.
RESULTS: Treatment with GA significantly improved the pathological changes in the liver and markedly decreased the positive area of Sirius red compared with rats in the CCl4-treated group. TUNEL assay showed that GA significantly reduced the number of TUNEL-positive cells compared with the CCl4-treated group. The expression levels of cleaved caspase-3, Bax, α-SMA, CTGF, MMP2 and MMP9 proteins, and α-SMA mRNA, collagen type I and III mRNA were also significantly reduced by GA compared with the CCl4-treated group (P < 0.05).
CONCLUSION: GA treatment can ameliorate CCl4-induced liver fibrosis by inhibiting hepatocyte apoptosis and hepatic stellate cell activation.
Core tip: This study showed that glycyrrhizic acid (GA) had inhibitory effects on hepatocyte apoptosis and liver fibrosis, which were mainly associated with down-regulation of hepatic stellate cell (HSC) activation, thus regulating fibrotic-related factors, such as expression levels of connective tissue growth factor, MMP2 and MMP9 proteins, and collagen type I and III mRNA. Collectively, these results demonstrate that GA treatment significantly ameliorated CCl4-induced liver fibrosis by inhibiting hepatocyte apoptosis and HSC activation, which may provide potential therapeutic strategies for anti-fibrosis.