摘要
目的:观察红芪多糖对线粒体途径介导的膀胱癌细胞凋亡的影响,并探讨可能机制.方法:取对数期T24细胞,随机分为对照组(常规培养)、红芪多糖组(加入红芪多糖0.8 μg/L)、SP600125组(加入SP600125 10 μmol/L)、联合组(加入红芪多糖0.8 μg/L、SP600125 10 μmol/L).MTT法检测细胞增殖能力;双染法检测细胞凋亡率;JC-1法检测细胞线粒体损伤;免疫印迹法检测细胞相关蛋白表达.结果:与对照组比较,红芪多糖组24、48、72 h吸光度值、线粒体膜电位、B淋巴细胞瘤-2(Bcl-2)蛋白表达量降低;凋亡率,Bcl-2相关X蛋白(Bax)、半胱氨酸蛋白酶3(Caspase-3)蛋白表达量,p-c-Jun氨基末端激酶(JNK)/JNK、p-c-Jun/c-Jun升高(均P＜0.05),.SP600125组24、48、72 h吸光度值,线粒体膜电位、Bcl-2蛋白表达量升高;凋亡率,Bax、Caspase-3蛋白表达量,p-JNK/JNK、p-c-Jun/c-Jun降低(均P＜0.05).与红芪多糖组比较,联合组24、48、72 h吸光度值、线粒体膜电位、Bcl-2蛋白表达量升高;凋亡率,Bax、Caspase-3蛋白表达量,p-JNK/JNK、p-c-Jun/c-Jun降低(均P＜0.05).结论:红芪多糖可抑制膀胱癌T24细胞增殖,并通过介导线粒体途径促进其凋亡,作用机制可能与激活JNK/c-Jun信号通路有关.
Abstract
Objective:To observe the effects of Hedysarum polysaccharides(HPS)on the apoptosis of bladder cancer cells media-ted by mitochondrial pathway,and to explore the possible mechanism.Methods:T24 cells in log phase were collected and randomly divided into control group(conventional culture),Hedysarum polysaccharides group(adding Hedysarum polysaccharides 0.8 μg/L),SP600125 group(adding SP600125 10 μmol/L),and combination group(adding Hedysarum polysaccharides)0.8 μg/L,SP600125 10 μmol/L).MTT assay was used to detect cell proliferation.Double staining was used to detect the apoptosis rate.JC-1 method was used to detect mitochondrial damage in cells.Western blotting was used to detect expressions of cell-related proteins.Results:Compared with the control group,the absorbance values at 24,48 and 72 h,mitochondrial membrane potential,Bcl-2 pro-tein expression were decreased,apoptosis rate,expressions of Bax and Caspase-3 proteins,p-JNK/JNK,p-c-Jun/c-Jun were in-creased in the HPS group(P＜0.05),and the absorbance values at 24,48 and 72 h,mitochondrial membrane potential,Bcl-2 pro-tein expression were increased,apoptosis rate,expressions of Bax and Caspase-3 proteins,p-JNK/JNK,p-c-Jun/c-Jun were de-creased in the SP600125 group(P＜0.05).Compared with the HPS group,the absorbance values at 24,48 and 72 h,mitochondrial membrane potential,and Bcl-2 protein expression were increased,and apoptosis rate,expressions of Bax and Caspase-3 proteins,p-JNK/JNK,p-c-Jun/c-Jun were decreased in the combination group(P＜0.05).Conclusion:HPS can inhibit the proliferation of T24 cells and promote their apoptosis by mediating the mitochondrial pathway.The mechanism may be related to the activation of the JNK/c-Jun signaling pathway.
基金项目
河北省医学科学研究计划(2020)(20200936)
维普
万方数据