摘要
目的探究七叶皂苷钠对肝纤维化的作用及机制。方法通过四氯化碳诱导大鼠肝纤维化模型,治疗组给予七叶皂苷钠处理,通过HE、Masson染色及免疫组织化学染色检测模型组与治疗组大鼠肝组织胶原增生及纤维化程度。在细胞试验中,通过MTT、克隆形成实验检测HSC-T6细胞的生长增殖活性,通过流式细胞术检测HSC-T6细胞凋亡,通过蛋白免疫印迹检测HSC-T6细胞内蛋白表达情况。结果七叶皂苷钠使大鼠肝脏胶原纤维生成减少,纤维化减轻。七叶皂苷钠使HSC-T6细胞生长增殖抑制,蛋白表达降低,细胞凋亡增加。七叶皂苷钠抑制HSC-T6细胞内PI3K/AKT/mTOR通路和eIF4F复合物的形成。结论七叶皂苷钠通过PI3K/AKT/mTOR通路抑制eIF4F复合物的合成进而缓解大鼠肝纤维化的进展。
Objective To explore the effect and mechanism of sodium aescinate on liver fibrosis.Methods The liver fibrosis model of rats was induced by CCl4,and the treatment group was treated with sodium aescinate.The collagen and fibrosis degree of rat liver tissue were detected by HE,Masson staining and immunohistochemical staining.The growth and proliferation of HSC-T6 cells were detected by MTT and clone formation.The apoptosis of HSC-T6 cells was detected by flow cytometry,and protein expression in the cells was detected by Western blot.Results Sodium aescinate decreased the production of collagen in the rat liver and reduced fibrosis.Sodium aescinate inhibited the growth and proliferation of HSC-T6 cells,reduced protein expression and increased cell apoptosis.Sodium aescinate inhibited the PI3K/AKT/mTOR pathway and eIF4F complex formation of HSC-T6 cells.Conclusion Sodium aescinate can inhibit the synthesis of eIF4F complex through PI3K/AKT/mTOR pathway and alleviate the progression of liver fibrosis in rats.
作者
谢海深
周大臣
李扬
崔笑
熊奇如
喻宗繁
Xie Haishen;Zhou Dachen;Li Yang(Dept of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601;Dept of Vascular Surgery, Taihe County People′s Hospital, Taihe 236600)
出处
《安徽医科大学学报》
CAS
北大核心
2021年第11期1733-1738,共6页
Acta Universitatis Medicinalis Anhui
基金
安徽省自然科学基金(编号:1808085MH270)。
