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银杏叶提取物可逆转四氯化碳诱导的大鼠肝纤维化。

Ginkgo biloba extract reverses CCl4-induced liver fibrosis in rats.

作者信息

Luo Yan-Jun, Yu Jie-Ping, Shi Zhao-Hong, Wang Li

机构信息

Department of Gastroenterology, Hubei Renmin Hospital, Wuhan University, Wuhan 430060, Hubei Province, China.

出版信息

World J Gastroenterol. 2004 Apr 1;10(7):1037-42. doi: 10.3748/wjg.v10.i7.1037.

Abstract

AIM

To study the reversing effect of Ginkgo biloba extract (GbE) on established liver fibrosis in rats.

METHODS

Following confirmation of CCl(4)-induced liver fibrosis, GbE or saline was administrated to the rats for 4 weeks. The remaining rats received neither CCl(4) nor GbE as normal control. The four groups were compared in terms of serum enzymes, tissue damage, expression of alphaSMA and tissue inhibitor-1 of metalloproteinase (TIMP-1) and metalloproteinase-1 (MMP-1).

RESULTS

Compared with saline-treated group, liver fibrosis rats treated with GbE had decreased serum total bilirubin (P<0.01) and aminotransferase levels (P<0.01) and increased levels of serum albumin (P<0.01). Microscopic studies revealed that the livers of rats receiving GbE showed alleviation in fibrosis (P<0.05) as well as expression of alphaSMA (P<0.01). The liver collagen and reticulum contents were lower in rats treated with GbE than saline-treated group (P<0.01). RT-PCR revealed that the level of TIMP-1 decreased while the level of MMP-1 increased in GbE group.

CONCLUSION

Administration of GbE improved CCl(4)-induced liver fibrosis. It is possibly attributed to its effect of inhibiting the expression of TIMP-1 and promoting the apoptosis of hepatic stellate cells.

摘要

目的

研究银杏叶提取物(GbE)对大鼠已形成的肝纤维化的逆转作用。

方法

在确认四氯化碳诱导的肝纤维化后,给大鼠施用GbE或生理盐水,持续4周。其余大鼠既不接受四氯化碳也不接受GbE作为正常对照。比较四组大鼠的血清酶、组织损伤、α平滑肌肌动蛋白(alphaSMA)的表达以及金属蛋白酶组织抑制剂-1(TIMP-1)和金属蛋白酶-1(MMP-1)的水平。

结果

与生理盐水处理组相比,用GbE处理的肝纤维化大鼠血清总胆红素降低(P<0.01),转氨酶水平降低(P<0.01),血清白蛋白水平升高(P<0.01)。显微镜研究显示,接受GbE的大鼠肝脏纤维化减轻(P<0.05),alphaSMA表达降低(P<0.01)。用GbE处理的大鼠肝脏胶原蛋白和网状纤维含量低于生理盐水处理组(P<0.01)。逆转录聚合酶链反应(RT-PCR)显示,GbE组TIMP-1水平降低,而MMP-1水平升高。

结论

施用GbE可改善四氯化碳诱导的肝纤维化。这可能归因于其抑制TIMP-1表达和促进肝星状细胞凋亡的作用。

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