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Lack of Cardioprotection by DCA Against TNFα-Induced Apoptosis in Cardiac Myocytes

This figure presents results showing that treatment with 1.5mM DCA did not improve apoptotic signaling induced by 100ng/mL TNFα in serum-starved H9c2 cardiac myocytes. Levels of Bax, Bcl-2 Expression, and cleaved caspase-3 were similar to TNFα-treated controls. Results represent 1 experiment out of 4.

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Lack of Cardioprotection by DCA Against TNFα-Induced Apoptosis in Cardiac Myocytes

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  1. Supplementary Figure 1 3 hr 1 hr 24 hr Control + 1x PBS Control + 1.5 mM DCA TNFα (100 ng/mL) 1x PBS TNFα (100 ng/mL) 1.5 mM DCA Co-Treat with TNFα Harvest Cells Serum Starve Cells Treat Cells with DCA Actin P-PDH PDH Bax Bcl-2 Cleaved Caspase 3 Supplementary Figure 1. DCA does not protect cardiac myocytes against TNFα-induced apoptosis. H9c2 cardiac myocytes were serum starved for 3 hrs, and then treated with 1.5 mM DCA. 1 hr into DCA treatment, 100 ng/mL TNFα was added to the culture medium for 24 hrs to induce apoptosis. DCA-mediated activation of PDH did not improve apoptotic signaling in response to TNFα, as Bax expression, Bcl-2 expression, and caspase 3 cleavage levels were similar to those observed in TNFα treated control cardiac myocytes. Scans represent 1 experiment out of 4.

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