Figure 3: Characterizing Changes in Mitochondrial Function and Cell Energetics With Sunitinib Treatment
2019-06-11T07:08:49Z (GMT) by
(A) Flow cytometry histogram showing levels of tetramethylrhodamine (TMRM). Neonatal rat ventricular myocytes grown in flat culture were treated with 0.1% dimethyl sulfoxide (vehicle), 1 μmol/l sunitinib, or 50 μmol/l carbonyl cyanide m-chlorophenyl hydrazine (CCCP) for 30 min (CCCP) or 4 h (dimethyl sulfoxide and sunitinib) and then were labeled with 10 nmol/l TMRM. (B) Time-dependent decreases in mitochondria membrane potential following treatment with 1 μmol/l sunitinib. Neonatal rat ventricular myocytes grown in flat culture were treated with 0.1% dimethyl sulfoxide or 1 μmol/l sunitinib for 30 min to 24 h and labeled with TMRM to assess mitochondria membrane potential. *p < 0.05 (n = 3 experiments). (C) Decreases in adenosine triphosphate (ATP) levels in neonatal rat ventricular myocytes following 24 h treatment with 1 μmol/l sunitinib. *p < 0.05 (n = 3 experiments). (D) Upstream activation of adenosine monophosphate-activated protein kinase with molecule 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) did not reverse sunitinib-induced caspase activation in rat cardiac microtissues (n = 2 experiments). NS = not significant.