Butein protects from PC12 cells apoptosis induced by methylglyoxal via inhibiting p53 signaling pathway
10.3969/j.issn.1001-1978.2018.05.008
- VernacularTitle: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
- Author:
Liang LE
1
;
Jiang XU
;
Bao-Ping JIANG
;
Li-Jia XU
;
Ke-Ping HU
;
Shi-Lin CHEN
;
Pei-Gen XIAO
Author Information
1. 中国医学科学院北京协和医学院药用植物研究所
- Keywords:
butein;
methylglyoxal;
PC12 cells;
apop-tosis;
p53;
caspase-9
- From:
Chinese Pharmacological Bulletin
2018;34(5):620-626
- CountryChina
- Language:Chinese
-
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.
