Role of RISK signal pathway in reducing cardiomyocytes hypoxia/reoxygenation injury induced by S1 P postconditioning
10.3969/j.issn.1001-1978.2015.02.008
- VernacularTitle:RISK信号通路在1-磷酸鞘氨醇后适应减轻心肌细胞缺氧/复氧损伤中的作用
- Author:
Yuqing WANG
;
Yanna WU
;
Xin LI
;
Yongqiang YIN
;
Yi KANG
;
Jianshi LOU
;
Ke WEN
- Publication Type:Journal Article
- Keywords:
S1 P;
hypoxia/reoxygenation;
H9 c2 cells;
PI3 K/Akt;
ERK1/2;
RISK
- From:
Chinese Pharmacological Bulletin
2015;(2):181-185
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the protective effects of sphingosine 1-phosphate (S1P) postconditioning on rat myocardial cells injured by hypoxia/reoxygenation in reperfusion injury salvage kinase ( RISK ) signal path-way. Methods The cultured rat H9c2 cells were ran-domly divided into seven groups: ( 1 ) control group;(2) hypoxia/reoxygenation (H/R) group; (3) S1P group;(4) S1P+LY294002 group(S1P+LY); (5) LY group; ( 6 ) S1 P +PD98059 group ( S1 P +PD );(7) PD group. The viability of H9c2 cells was detec-ted using MTT method. The content of MDA in the cultured medium and the activity of T-SOD and Mn-SOD were measured with colorimetry. The concentra-tion of intracellular free calcium ion was detected by confocal microscopy. The rate of cell apoptosis was de-termined by flow cytometric analysis. Western blot was used to assess phosphorylation of Akt and ERK1/2 in H9c2 cells. Results Compared with the H/R group, S1P significantly increased vaibility of cells, lowered the rate of apoptosis, decreased the content of MDA in the culture medium, increased the activity of T-SOD and Mn-SOD, reduced concentration of intracellular calcium and increased the phosphorylation of Akt and ERK1/2 . When added LY294002 or PD98059 , the effects of S1P above were inhibited. Conclusion S1P protects H9 c2 cells against hypoxia/reoxygenation inju-ry. The protection of S1P was inhibited by LY294002, the inhibitor of PI3 K/Akt and PD98059 , the inhibitor of ERK1/2 . S1 P protects H9 c2 cells against hypoxia/reoxygenation injury via RISK pathway.
