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SAR7334增强紫杉醇对肝癌HepG2细胞敏感性的作用研究

唐杰 黄晓敏 亢鹏举 史丹丹 贺细菊 冯娜

湖北医药学院学报2025,Vol.44Issue(5):532-538,555,后插1,9.
湖北医药学院学报2025,Vol.44Issue(5):532-538,555,后插1,9.DOI:10.13819/j.issn.2096-708X.2025.05.003

SAR7334增强紫杉醇对肝癌HepG2细胞敏感性的作用研究

Enhancement Effect of TRPC6-Specific Inhibitor SAR7334 in Sensitizing HepG2 Cells to Paclitaxel

唐杰 1黄晓敏 1亢鹏举 1史丹丹 1贺细菊 1冯娜1

作者信息

  • 1. 湖北医药学院基础医学院人体解剖学教研室,湖北 十堰 442000
  • 折叠

摘要

Abstract

Objective To explore the enhancement effect of TRPC6-specific inhibitor SAR7334 in sensitizing HepG2 cells to paclitaxel(PTX).Methods HepG2 cells were cultured in vitro and treated with PTX alone or in combination with SAR7334.Cell proliferation and apoptosis were assessed using CCK-8,RTCA,and Hoechst staining.JC-1 and MitoSOX fluorescent probes were employed to detect changes in mitochondrial membrane potential and reactive oxygen species(ROS)levels,respectively.Western blot was performed to analyze the expressions of apoptosis-related proteins(Bcl-2,Bax,Bad)and signaling pathway proteins(p-AKT,p-GSK-3β).Results Compared with monotherapy groups,the com-bination treatment significantly inhibited HepG2 cell viability,reduced mitochondrial membrane potential,and increased ROS levels(P<0.05).Western blot analysis demonstrated that the expression levels of pro-apoptotic proteins Bax and Bad were up-regulated in the combination group,while the phosphorylation levels of anti-apoptotic protein Bcl-2 and the AKT/GSK-3β pathway were decreased.Conclusion TRPC6-specific inhibitor SAR7334 effectively enhances the anti-prolifera-tive and pro-apoptotic effects of PTX in HepG2 cells,potentially through inhibiting the activation of AKT/GSK-3β path-way.

关键词

TRPC6/SAR7334/紫杉醇/增殖/凋亡

Key words

TRPC6/SAR7334/Paclitaxel/Proliferation/Aapoptosis

引用本文复制引用

唐杰,黄晓敏,亢鹏举,史丹丹,贺细菊,冯娜..SAR7334增强紫杉醇对肝癌HepG2细胞敏感性的作用研究[J].湖北医药学院学报,2025,44(5):532-538,555,后插1,9.

基金项目

湖北医药学院生物与医药学科群项目(2022BMXKQY3) (2022BMXKQY3)

十堰市引导性科研项目(24Y001) (24Y001)

湖北医药学院学报

2096-708X

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