中国药理学通报2018，Vol.34Issue(5)：620-626,7.DOI:10.3969/j.issn.1001-1978.2018.05.008
紫铆因通过抑制p53信号通路对抗丙酮醛诱导的PC12细胞凋亡
Butein protects from PC12 cells apoptosis induced by methylglyoxal via inhibiting p53 signaling pathway
摘要
Abstract
Aim To study the effect of butein on apop-tosis of PC12 cells induced by methylglyoxal (MG) and its mechanism. Methods Being pretreated with different concentrations of butein, PC12 cells were damaged by 1.5 mmol·L-1MG. Cell viability and cell toxicity were evaluated by MTT and LDH assay. Cell apoptosis and death were analyzed by PI and Ho-echst 33342. The antioxidant gene and proapoptotic gene expressions were determined by RT-PCR. The protein expression of p53 was detected by Western blot. Results Being pretreated with 2.5~10 μmol· L-1butein for 1 h significantly increased the cell via-bility,decreased LDH release,and protected from cell nuclei shrinkage, condensation and cleavage by MG. Meanwhile, butein increased the gene expression of SOD2, decreased the gene expression of proapoptotic genes p53 and caspase-9, and lowered the protein ex-pression of p53. Conclusion Butein can protect ap-optosis of PC12 cells from MG in a dose-dependent manner,which is linked with antioxidation and inhibi-ting p53 and caspase-9 gene expression.关键词
紫铆因/丙酮醛/PC12细胞/凋亡/p53/caspase-9Key words
butein/methylglyoxal/PC12 cells/apop-tosis/p53/caspase-9分类
医药卫生引用本文复制引用
乐亮,徐江,姜保平,许利嘉,胡克平,陈士林,肖培根..紫铆因通过抑制p53信号通路对抗丙酮醛诱导的PC12细胞凋亡[J].中国药理学通报,2018,34(5):620-626,7.基金项目
国家自然科学基金资助项目(No 81703223,81573576) （No 81703223,81573576）
中国博士后科学基金资助项目(No 2017M611127) （No 2017M611127）
