p38MAPK信号转导通路在七氟烷后处理减轻乳鼠心肌细胞缺氧复氧损伤中的作用

Objective To evalnate the role of p38 mitogen-activated protein kinase (p38MAPK) signal pathway in the protective effect of sevoflurane postconditioning (S-Postcon) on cultured neonatal rat cardiomyocytes against anoxia/reoxygenation (A/R) injury. Methods Primary cultured neonatal rat cardiomyocytes were randomly divided into 7 groups: group Ⅰ normal control (C); group Ⅱ A/R; group Ⅲ S-Poatcan + A/R; group ⅣS-Postcon + SB203580 + A/R; group Ⅴ S-Postcon + DMSO + A/R; group Ⅵ SB203580 + A/R and group Ⅶ DMSO + A/R. GroupⅡ-Ⅶ were exposed to 2 h anoxia (95% N2-5% CO2) followed by 1 h reoxygenation. In group Ⅲ, Ⅳ and Ⅴ the cultured myocytes were postconditioned with 20 min 3% sevoflurane in 97% O2 alone (in group Ⅲ) or in conjunction with 5 μmol/L 5B203580 (a specific p38 MAPK inhibitor) (in group Ⅳ) or 0.1% DMSO (in group Ⅴ) followed by 40 min reoxygenation. The cardiomyocytes were reoxygenated in the presence of 5 μmol/L SB203580 in group Ⅵ or 0.1% DMSO in group Ⅶ. The LDH activity, cell survival rate and apoptotic rate were measured at the end of the experiment. The levels of phosphor-p38MAPK (p-p38MAPK) was detected by Western blotting. Results S-Postcon reduced LDH activity and apoptotic rate and increased cell survival rate and the level of p-p38MAPK as compared with group A/R (group Ⅱ). The myocardial protecfive effect of S-Posteon was eliminated by p38MAPK inhibltor-SB203580 and p-p38MAPK level was also decreased at the same time.Conclusion Sevoflurane postconditioning can attenuate anoxia/reoxygenation induced cardiomyocyte injury through activation of p38MAPK signal pathway.

The role of p38 mitogen-activated protein kinase pathway in protective effect of sevoflurane postconditioning on cultured neonatal rat cardiomyocytes against anoxia/reoxygenafion injury