RESUMO
Objective: To investigate the effect of CrkL silence on hypoxia/reoxygenation (H/R)-induced apoptosis and survival inhibition in cardiomyocytes and the underlying mechanisms. Methods: H9C2 cardiomyocytes were infected with blank, negative lentivirus and CrkL RNAi lentivirus (CrkL mRNA silence), and then treated with H/R separately. The cardiomyocytes were divided into blank group, negative lentivirus group, CrkL silence group, blank + H/R group, negative lentivirus + H/R group and CrkL silence + H/R group. The expression of CrkL mRNA was detected by RT-PCR, and the expression of CrkL and p-ERK1/2 protein was detected by Western blotting analysis. The apoptosis rate of cardiomyocytes was analyzed by flow cytometry, and the cell proliferation rate was analyzed by MTT. Results: Compared with blank and negative lentivirus groups, CrkL silence group had significantly decreased CrkL mRNA and protein, p-ERK1 protein, p-ERK1/2 protein and proliferation rate (P<0.05 or P<0.01), and significantly increased apoptosis rate (P<0.01). The same was true for CrkL silence + H/R group when compared with the blank + H/R and negative lentivirus + H/R groups. Conclusion: CrkL silence can aggravate H/R-induced apoptosis and survival inhibition in cardiomyocytes, which might be mediated by the decrease of p-ERK1/2 protein expression.
RESUMO
Objective To study the expression and clinical significance of COX-2 and the relation- ship between COX-2 and PTEN in endometrial adenocarcinoma(EAC).Methods The expression of COX-2, PTEN protein was detected by SP-immunohistochemical method in EAC,endometrial intraepithelial neoplasia, corresponding normal endometrium.Results The positive rates of COX-2 protein increased from normal en- dometrium(13.33%) to endometrial intraepithelial neoplasia(50.00%) and adenocarcinoma(64.58 %)(P