五味子乙素通过靶向 TGF-β 信号通路抑制 miR-101-5p 抑制大鼠肝纤维化。

Schisandrin B suppresses liver fibrosis in rats by targeting miR-101-5p through the TGF-β signaling pathway.

机构信息

Key Laboratory Breeding Base of Hunan Oriented Fundamental and Applied Research of Innovative Pharmaceutics, Department of Basic Medical Science, Changsha Medical University, Changsha, China.

出版信息

Artif Cells Nanomed Biotechnol. 2020 Dec;48(1):473-478. doi: 10.1080/21691401.2020.1717507.

DOI:10.1080/21691401.2020.1717507

PMID:31975615

Abstract

Schisandrin B (Sch B) and miR-101 family members play critical roles in the pathogenesis of liver fibrosis. However, the relationship between them has not been reported yet. Thus, this study aims to fill this research gap. Results showed that Sch B significantly upregulated the expression of miR-101-5p in HSC-T6 cells. Sch B also increased the expression of miR-101-5p by combined administration of TGF-β1 and Sch B. Using miR-101-5p inhibitor, we demonstrated that Sch B can target miR-101-5p through the TGF-β signalling pathway to regulate the proliferation and activation of HSC-T6 cells. A rat model of carbon tetrachloride-induced liver fibrosis was established, and results indicated that Sch B can attenuate liver fibrosis by upregulating the expression of miR-101-5p. In conclusion, Sch B can directly target miR-101 to suppress liver fibrosis. Sch B or miR-101-5p may be used as a therapeutic approach for the prevention and treatment of liver fibrosis.

摘要

五味子丙素（Sch B）和 miR-101 家族成员在肝纤维化的发病机制中起着关键作用。然而，它们之间的关系尚未报道。因此，本研究旨在填补这一研究空白。结果表明，Sch B 可显著上调 HSC-T6 细胞中 miR-101-5p 的表达。Sch B 还通过联合给予 TGF-β1 和 Sch B 增加 miR-101-5p 的表达。使用 miR-101-5p 抑制剂，我们证明 Sch B 可以通过 TGF-β 信号通路靶向 miR-101-5p 来调节 HSC-T6 细胞的增殖和激活。建立了四氯化碳诱导的大鼠肝纤维化模型，结果表明 Sch B 可以通过上调 miR-101-5p 的表达来减轻肝纤维化。总之，Sch B 可以直接靶向 miR-101 抑制肝纤维化。Sch B 或 miR-101-5p 可能作为预防和治疗肝纤维化的治疗方法。