OBJECTIVE: Ischemia-reperfusion (IR) injury remains an unresolved and complicated situation in clinical practice. In this study, H9c2 cardiomyocytes were subjected to curcumin (Cur) treatment in the absence or presence of the silent information regulator 3 (SIRT3) inhibitor 3-TYP and were then subjected to IR. MATERIALS AND METHODS: H9c2 cells and male Sprague-Dawley (SD) rats were cultured. MTT assay was performed to assess H9c2 cell viability. Cellular apoptosis was analyzed by TUNEL assay. The expressions of Bcl-2, Bax, SIRT3, and AcSOD2 were measured by Western-blotting. The activities of SOD, GSH-Px, and MDA were determined using commercially available kits. The myocardial infarct size was evaluated using TTC staining. RESULTS: Cur significantly increased H9c2 cell viability, decreased the cell apoptotic index, and altered several biochemical parameters, including upregulation of the anti-apoptotic protein Bcl-2, downregulation of the proapoptotic protein Bax and AcSOD2, activation of SIRT3, increase in SOD and GSH-Px activity, and decrease in MDA content. In isolated rat hearts, Cur significantly improved cardiac function, decreased infarct size, and lowered lactate dehydrogenase levels. These protective effects induced by Cur were reversed by treatment with the SIRT3 inhibitor 3-TYP. CONCLUSIONS: These results demonstrate that Cur protects cardiomyocytes and that rat hearts were exposed to IRI by activating SIRT3.
OBJECTIVE:Ischemia-reperfusion (IR) injury remains an unresolved and complicated situation in clinical practice. In this study, H9c2 cardiomyocytes were subjected to curcumin (Cur) treatment in the absence or presence of the silent information regulator 3 (SIRT3) inhibitor 3-TYP and were then subjected to IR. MATERIALS AND METHODS: H9c2 cells and male Sprague-Dawley (SD) rats were cultured. MTT assay was performed to assess H9c2 cell viability. Cellular apoptosis was analyzed by TUNEL assay. The expressions of Bcl-2, Bax, SIRT3, and AcSOD2 were measured by Western-blotting. The activities of SOD, GSH-Px, and MDA were determined using commercially available kits. The myocardial infarct size was evaluated using TTC staining. RESULTS: Cur significantly increased H9c2 cell viability, decreased the cell apoptotic index, and altered several biochemical parameters, including upregulation of the anti-apoptotic protein Bcl-2, downregulation of the proapoptotic protein Bax and AcSOD2, activation of SIRT3, increase in SOD and GSH-Px activity, and decrease in MDA content. In isolated rat hearts, Cur significantly improved cardiac function, decreased infarct size, and lowered lactate dehydrogenase levels. These protective effects induced by Cur were reversed by treatment with the SIRT3 inhibitor 3-TYP. CONCLUSIONS: These results demonstrate that Cur protects cardiomyocytes and that rat hearts were exposed to IRI by activating SIRT3.