RESUMO
AIM:To investigate the influence of programmed cell death 5 (PDCD5) on apoptosis and autoph-agy in the cardiomyocytes exposed to hypoxia/reoxygenation ( H/R) and its potential mechanism .METHODS:H9c2 cells were exposed to H/R.PDCD5 was downregulated by RNA interference .The cell viability was measured by MTT assay . TUNEL assay was used to detect cell apoptosis .The mRNA and protein levels were determined by RT-qPCR and Western blot.RESULTS:The expression of PDCD5 was upregulated in the cardiomyocytes after H/R injury.Furthermore, H/R injury obviously reduced the cell viability and enhanced the apoptosis and autophagy of the cardiomyocytes .However, knockdown of PDCD5 increased the cell viability , and attenuated H/R-induced apoptosis , accompany with reduction of Bax and augment of Bcl-2 expression .Additionally , silencing PDCD5 markedly inhibited H/R-induced autophagy by regulating the expression of LC3-II/LC3-I and beclin-1.Moreover, downregulation of PDCD5 suppressed NF-κB signaling by redu-cing the protein level of p-P65.CONCLUSION: Silencing PDCD5 suppresses H/R-induced H9c2 cells apoptosis and autophagy by blocking NF-κB signaling pathway .The result indicates a new strategy for the prevention and treatment of myocardial I/R injury.