Effect of emulsified isoflurane on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytes

摘要

Objective:To explore the effect of emulsified isoflurane(EI) on apoptosis of anoxia-reoxygenation neonatal rat cardiomyocytes and relevant protein expression.Methods:Cardiac muscle anoxia-reoxygenation damage model was established with culture in vitro neonatal rat cardiomyocytes. The cardiomyocytes were divided into control group, model group, fat emulsion group andEI group.The cardiomyocytes apoptosis rates and lactic dehydrogenase(LDH), superoxide dismutase (SOD) and malondialdehyde(MDA) index standardization were detected after relevant treatment. The expression of apoptosis-related proteinsBel-2,Bax andCaspase-3 were detected with Western blot approach.Results:After hypoxia/reoxygenation(H/R) model was treated byEI, the cells apoptosis rate decreased and was dramatically below the fat emulsion group(P<0.05). Cardiomyocytes biochemical index detection presented that, compared with the control group that theLDH activity andMDA content dramatically increased(P<0.05), while theSOD activity notably decreased(P<0.05); compared with theH/R group, theSOD activity of the fat emulsion group and EI group increased(P<0.05); while theLDH activity andMDA content decreased(P<0.05).And the change of theEI group was more remarkable than the fat emulsion group(P<0.05).TheWestern blot analysis presented that, compared with the control group, theBcl-2 protein expression of the other groups significantly decreased(P<0.05), the expressions ofBax protein andCaspase-3 protein increased significantly(P<0.05); compared withH/R group, cardiomyocytesBcl-2 protein expression ofEI group increased significantly(P<0.05), the expressions ofBax protein andCaspase-3 protein decreased significantly(P<0.05), and the change ofEI group was more remarkable than the fat emulsion group(P<0.05).Conclusions:EI can inhabit the apoptosis of anoxia-reoxygenation damage model cardiomyocytes, and may be related to the up-regulation of expression ofBcl-2 and down-regulation of expression ofCaspase-3 protein.