Effect of hypoxic postconditioning and diazoxide postconditioning on calreticulin expression during hypoxia/reoxygenation in rat cardiomyocytes
10.3760/cma.j.issn.0254-1416.2010.11.024
- VernacularTitle:缺氧后处理和二氮嗪后处理对大鼠心肌细胞缺氧复氧时钙网蛋白表达的影响
- Author:
Gang YAO
;
Chi CHENG
;
Lin ZHANG
;
Shengli DENG
;
Xingkui LIU
;
Tian YU
- Publication Type:Journal Article
- Keywords:
Anoxia;
Diazoxide;
Cell hypoxia;
Oxygen;
Calreticulin
- From:
Chinese Journal of Anesthesiology
2010;30(11):1361-1363
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of hypoxic postconditioning and diazoxide postconditioning on the calreticulin expression during hypoxia/reoxygenation (H/R) in rat cardiomyocytes. Methods Primary cultured male SD rat cardiomyocytes were randomly divided into 6 groups (n = 8 each): control group (group C),H/R group; hypoxic postconditioning group (group HP) and diazoxide postconditioning group (group DP). Group C were cultured continuously for 2 h. Group H/R, Hp and DP were exposed to 45 min hypoxia (95% N2-5% CO2)followed by 1 h reoxygenation. In group HP, the cells were subjected to three cycles of 3 min hypoxia at 3 min intervals at the end of 45 min hypoxia before 1 h reoxygenation. In group DP, diazoxide 50 μmol/L was giyen at the end of hypoxia. Caspase-3 activity, calreticulin expression and intracellular free calcium ion concentrations were determined. Results Compared with group C, caspase-3 activity was significantly increased in the other groups,the calreticulin expression was up-regulated in group HP and DP, and the free calcium ion concentrations were increased in group H/R (P ＜ 0.05 or 0.01). Compared with group H/R, caspase-3 activity was significantly decreased in HP and DP, the calreticulin expression was up-regulated and the free calcium ion concentrations were decreased in group HP and DP (P ＜ 0.01). Conclusion Hypoxic postconditioning and diazoxide postconditioning attenuate H/R injury in rat cardiomyocytes through up-regulating the expression of calreticulin and reducing intracellular calcium overload.
