Cardioprotective Effect of Pinitol Against Streptozotocin-Diabetic Cardiomyopathy in Rats: Role of ANP, BNP, cTn-I and Apoptosis

Abstract

Diabetic cardiomyopathy (DCM) is a serious, complicated, and one of the most prevalent
metabolic complications of the cardiovascular system associated with diabetes mellitus patients. D-pinitol
is a naturally occurring compound well known for its antidiabetic, anti-inflammatory, and antioxidant potential. The aim of present investigation was to determine the potential of pinitol against streptozotocin
(STZ)-induced DCM in experimental animals diabetes was induced in Sprague-Dawley rats (200-250g) by
the administration of STZ (55 mg/kg, i.p.). After weeks of confirmation of diabetes, animals were treated
with pinitol (5, 10, and 20 mg/kg, p.o.), and various left ventricular, biochemical, and molecular parameters were evaluated. Intraperitoneal administration of STZ caused significant (p < 0.05) induction of DCM
reflected by alterations in electrocardiographic, hemodynamic and left ventricular functions which were
significantly (p < 0.05) restored by pinitol (10 and 20 mg/kg) treatment. It also significantly (p < 0.05) attenuated STZ-induced alterations in CK-MB, LDH, insulin, and glycated hemoglobin levels. The decreased levels of cardiac SOD, GSH, Na-K-ATPase, and mitochondrial complex, whereas elevated levels of
cardiac MDA and NO after STZ administration were significantly (p < 0.05) restored by pinitol treatment.
Upregulated mRNA expression of cardiac ANP, BNP, cTn-I, Bcl2, and caspase3 was significantly (p <
0.05) inhibited by pinitol treatment. Pinitol also attenuated histopathological aberrations induced in cardiac tissue by STZ. In conclusion, pinitol exerts its cardioprotective efficacy via attenuation of cardiac
ANP, BNP, cTn-I, oxido-nitrosative stress, and apoptosis (Bcl2, and caspase3) expressions in diabetic rats.