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灵芝治疗可降低硫代乙酰胺诱导的小鼠肝纤维化。

Post-treatment of Ganoderma lucidum reduced liver fibrosis induced by thioacetamide in mice.

机构信息

Graduate Institute of Chinese Pharmaceutical Sciences, College of Pharmacy, China Medical University, 91 Hsueh Shih Road, Taichung, Taiwan, ROC.

出版信息

Phytother Res. 2010 Apr;24(4):494-9. doi: 10.1002/ptr.2949.

Abstract

The present study was aimed at assessing the effects of Ganoderma lucidum extract (GLE) on an established liver fibrosis model with reference to the previously reported hepatoprotective effect of GLE against CCl(4)-induced fibrosis in rats. Repeated administration of thioacetamide (TAA) for 12 weeks to mice induced liver fibrosis. Treatment with GLE after the induction of liver fibrosis decreased the hepatic hydroxyproline content and improved liver histology. RT-qPCR analysis showed that GLE treatment reduced the mRNA expression of collagen (alpha1)(I), smooth muscle alpha-actin, tissue inhibitor of metalloproteinase 1 and metalloproteinase-13. In addition, the TAA-induced decrease in total collagenase activity was reversed by GLE treatment. In conclusion, oral administration of GLE reversed TAA-induced liver fibrosis, the mechanism of which might be related to the enhancement of collagenase activity.

摘要

本研究旨在评估灵芝提取物(GLE)对已建立的肝纤维化模型的影响,参考先前报道的 GLE 对 CCl4 诱导的大鼠纤维化的保肝作用。用硫代乙酰胺(TAA)重复处理 12 周可诱导小鼠肝纤维化。肝纤维化诱导后给予 GLE 治疗可降低肝羟脯氨酸含量并改善肝组织学。RT-qPCR 分析显示,GLE 治疗可降低胶原(α1)(I)、平滑肌α-肌动蛋白、金属蛋白酶组织抑制剂 1 和金属蛋白酶-13 的 mRNA 表达。此外,GLE 治疗可逆转 TAA 诱导的总胶原酶活性降低。总之,口服 GLE 可逆转 TAA 诱导的肝纤维化,其机制可能与胶原酶活性增强有关。

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