Glycyrrhizic acid inhibits apoptosis and fibrosis in carbontetrachloride-induced rat liver injury |
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Authors: | Bo Liang Xiao-Ling Guo Jing Jin Yong-Chun Ma Zheng-Quan Feng |
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Affiliation: | Bo Liang, Zheng-Quan Feng, Department of Oncology, Tongde Hospital of Zhejiang Province, Hangzhou 310012, Zhejiang Province, ChinaXiao-Ling Guo, Yong-Chun Ma, Department II of Psychosomatics, Tongde Hospital of Zhejiang Province, Hangzhou 310012, Zhejiang Province, ChinaJing Jin, Department of Ophthalmology, First People’s Hospital of Shanghai Jiaotong University, Shanghai 200080, China |
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Abstract: | 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. |
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Keywords: | Glycyrrhizic acid Hepatocyte apoptosis Liver fibrosis Hepatic stellate cell Matrix metalloproteinase |
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