Effect Of Crkl Silence On Hypoxia/Reoxygenation Induced Apoptosis And Surval Inhibition In Cardiomyocytes And Its Underlying Mechanism

Objective: To investigate the effect of CrkL silence onhypoxia/reoxygenation (H/R) induced apoptosis and survival inhibition incardiomyocytes and its underlying mechanisms.Methods: H9C2cardiomyocytes were infected with blank，negativelentivirus and CrkL RNAi lentivirus (CrkL mRNA silence)， then treatedwith H/R respectively. The cardiomyocytes were divided into blank group,negative lentivirus group, CrkL silence group, blank+H/R group, negativelentivirus+H/R group and CrkL slience+H/R group. The expression ofCrkL mRNA was detected by RT-PCR, and the expression of CrkL andp-ERK1/2protein was detected by Western blotting analysis. Theapoptosis rate of cardiomyocytes was analyzed by flow cytometry, and thecell proliferation rate was analyzed by MTT.Results: Compared with blank&negative lentivirus groups and blank+H/R&negative lentivirus+H/R groups, CrkL mRNA&protein,p-ERK1protein, p-ERK1/2protein and proliferation rate were significantly decreased（P<0.01，P<0.05）, and apoptosis rate was significantly increasedin the CrkL silence and CrkL silence+H/R groups respectively (P<0.01).Conclusions: CrkL silence can enhance H/R induced apoptosis andsurvival inhibition in cardiomyocytes, which might be mediated by thedecrease of p-ERK1/2protein expression.