Glycyrrhizic acid inhibits apoptosis and fibrosis in carbon-tetrachloride-induced rat liver injury
Glycyrrhizic acid inhibits apoptosis and fibrosis in carbon-tetrachloride-induced rat liver injury
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DOI：
10.3748/wjg.v21.i17.5271
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发表时间：
2015-05-07
影响因子：
4.3
通讯作者：
Feng, Zheng-Quan
中科院分区：
文献类型：
--
作者：
Liang, Bo;Guo, Xiao-Ling;Feng, Zheng-Quan
目的：目的：探讨甘草酸（GA）对四氯化碳（CCl 4）诱导肝纤维化的抗凋亡作用及其影响因素。苏木精-伊红染色观察大鼠肝脏病理变化。天狼星红染色检测胶原纤维。TUNEL法检测肝细胞凋亡，Western blot法检测caspase-3、Bax、α-SMA、结缔组织生长因子（CTGF）、基质金属蛋白酶（MMP）2、MMP 9蛋白表达，α-SMA mRNA、胶原蛋白表达。和.结果：与CCl 4处理组相比，GA处理组大鼠肝脏病理改变明显减轻，天狼猩红染色阳性面积明显减少。TUNEL法显示GA组TUNEL阳性细胞数较CCl 4组明显减少。Caspase-3、Bax、α-SMA、CTGF、MMP 2和MMP 9蛋白表达水平及α-SMA mRNA、胶原类型。和.结论：GA可通过抑制肝细胞凋亡和肝星状细胞活化，减轻CCl 4诱导的肝纤维化。
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, alpha-SMA, connective tissue growth factor (CTGF), matrix metalloproteinase (MMP) 2 and MMP9 proteins were evaluated by western blot analysis, and a-SMA mRNA, collagen type. and. 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, a-SMA, CTGF, MMP2 and MMP9 proteins, and a-SMA mRNA, collagen type. and. 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.