Department of Pharmacology, School of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Department of Pathology, School of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Biosci Biotechnol Biochem. 2021 Mar 24;85(4):775-785. doi: 10.1093/bbb/zbab001.
This research aimed to evaluate the antihepatic fibrosis effect and explore the mechanism of Qiwei Qinggan Powder (QGS-7) in vivo and in vitro. Carbon tetrachloride (CCl4)-treated rats and hepatic stellate cells (HSCs) were used. QGS-7 treatment significantly improved the liver function of rats as indicated by decreased serum enzymatic activities of alanine aminotransferase, aspartate transaminase, and alkaline phosphatase. Meanwhile, the hydroxyproline of liver was significantly decreased. Histopathological results indicated that QGS-7 alleviated liver damage and reduced the formation of fibrosis septa. Moreover, QGS-7 significantly attenuated expressions of Alpha smooth muscle actin, Collagen I, Janus kinase 2 (JAK2), phosphorylation-JAK2, signal transducer and activator of transcription 3 (STAT3), phosphorylation-STAT3 in the rat hepatic fibrosis model. QGS-7 inhibited HSC proliferation and promoted it apoptosis. QGS-7 may affect hepatic fibrosis through JAK2/STAT3 signaling pathway so as to play an antihepatic fibrosis role.
本研究旨在评估七味清肝粉（QGS-7）在体内和体外的抗肝纤维化作用，并探讨其作用机制。采用四氯化碳（CCl4）处理大鼠和肝星状细胞（HSCs）。结果表明，QGS-7 治疗可显著改善大鼠的肝功能，降低血清丙氨酸氨基转移酶、天冬氨酸转氨酶和碱性磷酸酶的酶活性。同时，肝羟脯氨酸含量明显降低。组织病理学结果表明，QGS-7 可减轻肝损伤，减少纤维隔的形成。此外，QGS-7 还显著下调了肝纤维化模型大鼠的 Alpha 平滑肌肌动蛋白、胶原 I、Janus 激酶 2（JAK2）、磷酸化-JAK2、信号转导和转录激活因子 3（STAT3）、磷酸化-STAT3 的表达。QGS-7 抑制 HSC 增殖并促进其凋亡。因此，QGS-7 可能通过 JAK2/STAT3 信号通路影响肝纤维化，从而发挥抗肝纤维化作用。
