XXXX protects the cardiocyte from @entity273 induced apoptosis in H9c2 cells.

@entity5568 @entity137 @entity522 @entity588 @entity39 @entity1836 @entity8187 @entity273 @entity35619 @entity3092 @entity65
OBJECTIVE: To elucidate the key parameters associated with @entity273 induced oxidative stress and investigates the mechanism of @entity35619 (TG) for reducing the @entity5568 induced @entity137 in H9c2 cells. METHODS: @entity137 and antioxidant activity of TG was assessed by EZ-CYTOX kit. RNA extraction and cDNA synthesized according to the kit manufacture protocol. Apoptosis was measured by the Flowcytometry, general PCR and qPCR. RESULTS: It was found that the TG significantly rescued the morphology of the H9c2 cells. Treatment of cells with TG attenuated @entity5568 induced cell deaths and improved the antioxidant activity. In addition, TG regulated the apoptotic gene @entity522 , @entity8187 and anti-apoptotic gene @entity588 , @entity1836 during @entity5568 induced oxidative stress in H9c2 cells. These results were comparable with @entity3092 treatment. For evident, flow cytometer results also confirmed the TG significantly reduced the @entity5568 induced @entity39 and apoptosis in H9c2 cells. However, further increment of TG concentration against @entity5568 could induce the @entity39 and apoptosis along with @entity5568 . CONCLUSIONS: It is suggested that less than 125   M of TG could protect the cells from @entity5568 induced cell damage by down regulating the caspases and up regulating the @entity588 and @entity1836 expression. Therefore, we suggest the @entity35619 could be useful for treatment of oxidative stress mediated @entity65 in future.
