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作 者:白新宇 孙士伟 王志鹏 尹跃伟 BAI Xinyu;SUN Shiwei;WANG Zhipeng;YIN Yuewei(Department of Urology,the 82nd Army Hospital,Baoding 071000,China;Department of Urology,the Second Hospital of Hebei Medical University,Shijiazhuang 050000,China)
机构地区:[1]陆军第八十二集团军医院泌尿外科,保定071000 [2]河北医科大学第二医院泌尿外科,石家庄050000
出 处:《世界中医药》2024年第7期980-984,共5页World Chinese Medicine
基 金:2020河北省医学科学研究计划项目(20200936)。
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0.8μg/L)、SP600125组(加入SP60012510μmol/L)、联合组(加入红芪多糖0.8μg/L、SP60012510μmol/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。Objective:To observe the effects of Hedysarum polysaccharides(HPS)on the apoptosis of bladder cancer cells mediated 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 0.8μg/L),SP600125 group(adding SP60012510μmol/L),and combination group(adding Hedysarum polysaccharides)0.8μg/L,SP60012510μmol/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 protein expression were decreased,apoptosis rate,expressions of Bax and Caspase-3 proteins,p-JNK/JNK,p-c-Jun/c-Jun were increased in the HPS group(P<0.05),and the absorbance values at 24,48 and 72 h,mitochondrial membrane potential,Bcl-2 protein expression were increased,apoptosis rate,expressions of Bax and Caspase-3 proteins,p-JNK/JNK,p-c-Jun/c-Jun were decreased 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.
关 键 词:红芪多糖 线粒体 膀胱癌 凋亡 Bcl-2相关X蛋白 C-JUN氨基末端激酶 半胱氨酸蛋白酶3
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