摘要
目的研究黄芩苷对人肝癌HepG2细胞增殖的抑制作用及其对p38MAPK信号通路的影响。方法以不同浓度的黄芩苷与人肝癌HepG2细胞共同培养24、48、72 h后,采用MTT法测定细胞增殖抑制率;通过活细胞计数,检测不同浓度黄芩苷处理后细胞活力的变化;采用western blotting方法检测黄芩苷处理72 h后HepG2细胞p38和p-p38蛋白的表达变化。结果黄芩苷对HepG2细胞生长有抑制作用,并随药物作用时间的延长和药物浓度的增加,其抑制效果越明显;通过对活细胞计数发现黄芩苷对HepG2细胞生长有抑制作用,随黄芩苷浓度的增加,细胞存活率下降,细胞增殖速度明显减缓;在黄芩苷处理72 h后p38蛋白表达兀明显变化,而p-p38蛋白表达上调且随黄芩苷浓度升高蛋白表达升高。结论黄芩苷可能通过激活p38MAPK信号通路诱导人肝癌HepG2细胞凋亡。
Objective To study the inhibitory effect of baicalin on the proliferation of human hepatic cancer HepG2 cells and relationship with p38MAPK signal pathway.Methods HepG2 cells were treated with different dosages of baicalin for 24-,48-and 72-h,and then the inhibitory rate of cell proliferation was detected by MTT assay.The change in cell vitality after treatment with different dosages of baicalin was determined by survival cell count assay.The expressions of p38 and p-p38 were determined by Western blotting.Results Baicalin had inhibitivc cffcct on the growth of HepG2 cells with different level,and with the increase in drug concentration or incubation time,the inhibitive effect became significant.The similar outcome was observed by survival cell count assay.HepG2 cells were incubated with baicalin for 72-h,and the expression of p-p38 increased compared with blank group while the expression of p38 had no obvious change.Conclusion Baicalin induces HepG2 apoptosis by activating p38MAPK signaling pathways.
出处
《临床军医杂志》
CAS
2015年第4期384-387,共4页
Clinical Journal of Medical Officers
