The Protective Role With its Mechanism of Lysophosphatidic Acid on Hypoxia/Re-Oxygenation Induced Neonatal Rat’s H9c2 Cardiomyocyte Injury

Objectives: To investigate the protective role with its mechanism of lysophosphatidic acid(LPA) on hypoxia/reoxygenation(H/R) induced neonatal rat’s H9c2 cardiomyocyte injury.Methods: The H/R model of neonatal rat’s H9c2 cardiomyocyte was established and the experiment was divided into 4 groups.Control group,with normal H9c2 cell.H/R group,no FBS cultured H9c2 cell was incubated in hypoxia condition for 24 hours and then cultured in 10% FBS-DMEM with routine oxygen concentration for 3 hours.H/R+LPA group and H/R+OMPT(LPA3 receptor agonist) group,the cells were treated by either LPA at(1,10,25)μM or OMPT at(1,5,10)μM for 1 hour respectively,then the cells received H/R procedures.The cell viability was examined by trypan blue staining,cell caspase-3/7 activity was detected with the commercial kit,cell apoptosis was measured by flow cytometry,and apoptotic proteins were analyzed by western blot analysis.Results: Compared with Control group,H/R group had decreased cell viability and increased early stage cell apoptosis,P0.05 respectively.Compared with H/R group,H/R+LPA group showed increased cell viability,P0.05,and LPA 10μM was the best,in addition,LPA(1,25)μM treated cells had decreased caspase-3/7 activity,P0.05.Compared with H/R group,H/R+OMPT group presented reduced Bax protein expression and elevated Bcl-2 protein expression,P0.05 or P0.01.Conclusion: LPA may protect H/R induced neonatal rat’s H9c2 cardiomyocyte injury by activating LPA3 receptor and suppressing the mitochondrial apoptotic pathway.