摘要
目的探讨土槿乙酸诱导的人卵巢癌细胞系HO-8910细胞自噬蛋白的表达及PI3K/Akt信号转导通路的变化,以及自噬特异性抑制剂3-甲基腺嘌呤(3-MA)和自噬激动剂雷帕霉素(RAPA)对自噬相关蛋白的影响。方法不同浓度的土槿乙酸作用HO-8910细胞,采用台盼蓝染色检测细胞的存活率,Western blot分析检测自噬相关蛋白及PI3K/Akt通路相关蛋白的变化,分别用3-MA和RAPA处理HO-8910细胞后检测自噬相关蛋白的变化。结果土槿乙酸能够诱导卵巢癌细胞HO-8910自噬,增加LC3-Ⅱ和自噬调节因子Beclin-1的表达;3-MA可以抑制土槿乙酸诱导的HO-8910细胞自噬相关蛋白的表达,而RAPA促进了土槿乙酸诱导的HO-8910细胞自噬相关蛋白的表达,且土槿乙酸能抑制PI3K/Akt通路蛋白的表达。结论土槿乙酸可通过抑制PI3K/Akt通路诱导HO-8910细胞自噬。
Objective To investigate the expression of autophagy proteins in human ovarian cancer HO-8910 cells induced by pseudolaric acid-B(PAB)and the changes in the PI3K/AKT pathway transduction,as well as the effects of 3-MA and RAPA on autophagy-related proteins.Methods The survival rate of HO-8910 was tested by Trypan blue staining after treatment with different concentration of Pseudolaric acid-B.Western blot analysis was used to detect the changes of autophagy-related proteins and PI3K/Akt pathway-related proteins.The changes of autophagy-related proteins were detected after treatment of HO-8910 cells with 3-MA and RAPA,respectively.Results Pseudolaric acid-B could induce autophagy of ovarian cancer cells HO-8910 and increase the expression of LC3-Ⅱ and autophagy regulatory factor Beclin-1.The 3-MA could inhibit the expression of autophagy-related protein of HO-8910 cell induced by pseudolaric acid-B,while RAPA could promote the expression.Pseudolaric acid-B inhibited the expression of PI3K/Akt pathway-related proteins.Conclusion Pseudolaric acid-B can induce autophagy of HO-8910 cells by inhibiting PI3K/Akt pathway.
作者
王佳贺
王楠
苑莉莉
WANG Jia-he;WANG Nan;YUAN Li-li(Department of Geriatrics,Shengjing Hospital of China Medical University,Shenyang 110004,China;Department of Gerontology and Geriatrics,Fifth Affiliated Hospital of Sun Yat-sen University,Zhuhai 519000,China;Department of Cardiology,Shenyang Red Cross Hospital,Shenyang 110013,China)
出处
《实用药物与临床》
CAS
2020年第9期792-795,共4页
Practical Pharmacy and Clinical Remedies
基金
沈阳市科技计划项目(18-013-0-57)。
