摘要
目的探讨黄芩苷对人肝癌Hep G2细胞生长的抑制作用及其对c-Jun氨基末端激酶(JNK)信号通路的影响。方法 50、100、150μg/ml的黄芩苷分别与人肝癌Hep G2细胞共同培养24、48和72 h,MTT测定细胞生长抑制率;采用Western blotting方法检测黄芩苷处理72 h后Hep G2细胞JNK和p-JNK的表达变化并观察JNK抑制剂对细胞凋亡的影响。结果黄芩苷对人肝癌Hep G2细胞增殖抑制作用呈时间依赖性,黄芩苷浓度低于100μg/ml其对细胞的抑制作用随浓度升高而增强,超过100μg/ml其对细胞的抑制作用不再增强。在黄芩苷处理后Hep G2细胞pJNK蛋白表达上调,使用JNK抑制剂后,能阻断JNK蛋白的磷酸化,并且降低黄芩苷诱导细胞凋亡的能力。结论黄芩苷通过激活JNK信号通路诱导人肝癌Hep G2细胞凋亡。
Objective To study the effects of Baicalin on inhibiting the proliferation of Hep G2 cells and c-jun n-terminal kinase（ JNK） signaling pathway in patients with hepatic cancer. Methods The 50,100 and 150 μg / ml of Baicalin were respectively cultured with Hep G2 cells for 24 h,48 h and 72 h,and then the inhibitory rate of cell proliferation was detected using MTT assay. The changes of Hep G2 cells and expressions of JNK and p-JNK after Baicalin treatment were detected using Western blotting,and the effect of JNK inhibitor on apoptosis was observed. Results The inhibitory effect of Baicalin on the proliferation of Hep G2 cells of patients with hepatic cancer was time dependence,and the inhibitory effect of Baicalin concentration was lower than 100 μg / ml on cell proliferation enhanced with the increased concentration,while the inhibitory effect of Baicalin concentration more than 100 μg / ml was not enhanced. The p-JNK protein expression in Hep G2 cells was increased after Baicalin treatment. After use of JNK inhibitor,the phosphorylation of JNK protein was blocked,and apoptotic ability induced by Baicalin was reduced. Conclusion Baicalin can induce Hep G2 apoptosis by activating JNK signaling pathways in patients with hepatic cancer.
出处
《解放军医药杂志》
CAS
2015年第4期20-23,共4页
Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
基金
江苏省淮安市产学研合作促进计划专项资金资助项目(HAC201026)
