紫杉醇通过p38MAPK通路对大鼠肾小管上皮细胞株自噬和凋亡的影响  

Influence of Taxol Passes Through the p38MAPK Pathway for Autophagy and Apoptosis in Rat Renal Tubular Epithelial Cells

作　　者：杨邱[1] 李亚[1] 李勇泉[1] 

机构地区：[1]深圳市人民医院内科,广东深圳518000

出　　处：《内蒙古医学杂志》2017年第7期779-780,F0004,共3页Inner Mongolia Medical Journal

摘　　要：目的探讨紫杉醇(Taxol)通过p38MAPK通路对体外培养的大鼠肾小管上皮细胞株(RPTC)自噬和凋亡的作用。方法体外培养的RPTC,将脂多糖(LPS)作为诱导剂,紫杉醇作为治疗物,分组进行检测自噬水平;分别用紫杉醇、p38MAPK抑制剂SB202190治疗LPS处理的RPTC,测定RPTC的自噬、凋亡和caspase活性。结果 Taxol能够通过降低p38磷酸化,上调LPS诱导的自噬水平,下调LPS诱导的RPTC凋亡。而SB202190逆转紫杉醇对LPS诱导的RPTC细胞凋亡的保护作用。结论紫杉醇可能通过抑制p38MAPK活化,上调LPS诱导的自噬,减少LPS诱导的RPTC凋亡。Objective To probe into the autophagy and apoptosis effects of Taxol passes through the p38MAPK pathway for rat renal tubular epithelial cells（RPTC） in vitro culture. Methods RPTC were cultured in vitro, and lipopolysaccharide（LPS） was used as inducer, Paclitaxel as the treatment agent, the the levels of au- tophagy were detected by grouping; The autophagy, apoptosis and caspase activity of RPTC were measured by the paclitaxel and p38MAPK inhibitor SB202190 in the treatment of LPS with RPTC. Results The Taxol which can reduce phosphorylation by p38, and raise the level of autophagy induced by LPS, and fall the LPS in- duced apoptosis in RPTC. While the SB202190 reverses the protective effect of paclitaxel on LPS induced apop- tosis in RPTC cells. Conclusion The Taxol could be through the inhibition of p38MAPK activation, and raise the autophagy induced by LPS, reduce the LPS induced apoptosis in RPTC.

关 键 词：凋亡 紫杉醇 P38MAPK LC-3 CASPASE-3 

分 类 号：R285.5[医药卫生—中药学]