SENP3 protects H9C2 cells from apoptosis triggered by H/R via STAT3 pathway.

OBJECTIVE:To investigate whether SENP3 protects H9C2 cells from apoptosis triggered by H/R through the signal transducer and activator of transcription 3 pathway. MATERIALS AND METHODS:Male C57BL mice were cultured and mouse models of myocardial I/RI were established. At the same time, cardiomyoblast H9C2 cell line of rat embryo was cultured. Reactive oxygen species level was detected during H/R using 2',7'-dichlorofluorescein diacetate (DCFH) kit. Apoptotic cells were checked by flow cytometry. The expressions of p-JAK2, JAK2, cleaved-caspase3 (c-caspase3), and Bcl/Bax were detected using Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS:We revealed that SENP3 rose in mice of I/R group and in H9C2 cells following H/R with an increase in Furthermore, increased expression of SENP3 was found to be dependent on the generation of as the SENP3 accumulation was inhibited by antioxidant (NAC). Inhibition of SENP3 suppressed the expression, but promoted cell apoptosis, c-caspase3 expression, and Bcl/Bax ratio. Besides, SENP3 overexpression alleviated the cell apoptosis, which was abrogated by AG490. CONCLUSIONS:SENP3 could protect H9C2 against H/R through enhancing pathway.

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