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作 者:花京剩 邵燕萍[3] 王石健[2] 罗爽[1] 陈蓉 刘恒芳 苗淑敏 HUA Jingsheng;SHAO Yanping;WANG Shijian(Department of Hematologic Oncology,Taizhou Municipal Hospital,Taizhou318000,CHINA)
机构地区:[1]台州市立医院血液肿瘤内科,浙江318000 [2]台州市立医院药剂科,浙江318000 [3]浙江省台州医院血液肿瘤内科
出 处:《江苏医药》2023年第10期973-976,F0002,共5页Jiangsu Medical Journal
基 金:台州市科技局项目(21ywb44)。
摘 要:目的探讨醉茄素A(WA)对肝癌细胞增殖、凋亡及侵袭的影响及其分子机制。方法分别采用WA 0、2、4、6、8μmol/L处理肝癌细胞株HepG2,MTT法检测细胞增殖,筛选出最佳作用浓度。再将HepG2细胞分为WA 0μmol/L组、WA 8μmol/L组和SP600125组[c-Jun氨基末端激酶(JNK)抑制剂SP60012520μmol/L预孵育1 h,再加入WA 8μmol/L],继续作用24或48 h。采用流式细胞术检测细胞凋亡,Transwell实验检测侵袭细胞数,反转录-聚合酶链反应和Western blot法分别检测磷酸化JNK(p-JNK)、JNK、Bax和Bcl-2的mRNA和蛋白表达。结果与WA 0μmol/L组比较,WA 8μmol/L组HepG2细胞凋亡率增加,侵袭细胞数减少,p-JNK、Bax mRNA和蛋白表达升高,Bcl-2的mRNA和蛋白表达降低(P<0.05);而预孵育SP600125后,上述作用被逆转(P<0.05)。结论WA能够抑制HepG2细胞增殖和侵袭,促进细胞凋亡,可能通过丝裂原活化蛋白激酶/JNK信号通路来实现。Objective To investigate the effects and molecular mechanism of withaferin A(WA)on the hepatocellular carcinoma cell proliferation,apoptosis and invasion.Methods The hepatocellular carcinoma cell line HepG2was treated with WA in diferent concentrations of 0,2,4,6 and 8μmol/L,respectively.MTT assay was used to detect cell proliferation and the optimal concentration was screened.HepG2cells were preincubated with WA 0μmol/L(group A),8μmol/L(group B)and c-Jun amino-terminal kinase(JNK)inhibitor SP60012520μmol/L(group C)for 1hour,and then group C was treated with WA 8μmol/L for 24or 48hours.The cell apoptosis was detected by flow cytometry,the number of invasive cells was detected by Transwell assay,and the mRNA and protein expressions of phosphorylated JNK(p-JNK),JNK,Bax and Bcl-2were detected by reverse transcriptase polymerase chain reaction and Western blot.Results Compared with WA 0μmol/L,WA 8μmol/L promoted cell apoptosis,inhibited cell invasion,increased mRNA and protein expressions of p-JNK and Bax,decreased mRNA and protein expressions of Bcl-2(P<0.05).The above effects were reversed when preincubated with SP600125(P<0.05).Conclusion WA can inhibit proliferation and invasion of HepG2cells and promote apoptosis.The mechanism for that is possibly through mitogen-activated protein kinase/JNK signaling pathway.
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