Quercetin and vitamin E ameliorate cardio-apoptotic risks in diabetic rats.

Apoptosis is upregulated in all forms of diabetes, and the mitochondria act as target in diabetes pathophysiology. Quercetin and vitamin E have both shown usefulness in the delay of progression of diabetes-induced complications. However, their effect on the apoptotic process in diabetes mellitus is unknown. We hypothesize that quercetin treatment in diabetes may decrease the propensity for cardiomyocytic death via regulation of the mitochondria permeability transition (mPT) pore opening. Hearts from normal and streptozotocin-induced diabetic rats were used for the study. Low ionic strength heart mitochondria were used for swelling assay and mitochondrial lipid peroxidation (mLPO) activity was spectrophotometrically assessed. Levels of cytochrome c and caspase 3 and 9 were determined by immunohistochemistry, while lesions assessed by histology. Diabetic heart mPT pore showed larger amplitude swelling than control, while mLPO levels were increased in diabetic rats relative to control, this resulted in cytochrome c release. This initiated increased caspase 3 and 9 activity in diabetic rats (p < 0.05). Histology showed hemorrhagic lesions in diabetic rat hearts. Quercetin and vitamin E treatment reversed these effects, suggestive of their anti-apoptotic effect. Quercetin and vitamin E protection in diabetes is mediated by mPT pore inhibition and modulation of mitochondrial-mediated apoptosis.