Salau_2022_Fundam.Clin.Pharmacol_30_12522

BACKGROUND: Cardiovascular abnormalities have been reported as a major contributor of diabetic mortality. The protective effect of ferulic acid on diabetic cardiomyopathy in fructose-streptozotocin induced type 2 diabetic (T2D) rat model was elucidated in this study. METHODS: T2D rats were treated by oral administration of low (150 mg/kg b.w) and high (300 mg/kg b.w) doses of ferulic acid. Metformin was used as the antidiabetic drug. Rats were humanely euthanized after 5 weeks of treatment and their blood and hearts were collected. RESULTS: Induction of T2D depleted the levels of reduced glutathione, glycogen, HDL-cholesterol and the activities of superoxide dismutase, catalase, ENTPDase and 5'Nucleotidase. It simultaneously triggered marked increase in levels of malondialdehyde, total cholesterol, triglyceride, LDL-cholesterol, creatinine kinase-MB as well as activities of acetylcholinesterase, ACE, ATPase, Glucose-6-phopsphatase, fructose-1,6-bisphophatase, glycogen phosphorylase and lipase. T2D induction further revealed obvious degeneration of cardiac muscle morphology. However, treatment with ferulic acid markedly reversed the levels and activities of these biomarkers with concomitant improvement in myocardium structural morphology, which had favourable comparison with the standard drug, metformin. Additionally, T2D induction led to depletion of 40, 75, and 33% of fatty acids, fatty esters, and steroids, respectively with concomitant generation of eicosenoic acid, gamolenic acid and vitamin E. Ferulic acid treatment restored eicosanoic acid, 2-hydroxyethyl ester, with concomitant generation of 6-Octadecenoic acid, (Z)-, cis-11-Eicosenoic acid, tridecanedioic acid, octadecanoic acid, 2-hydroxyethyl ester, ethyl 3-hydroxytridecanoate, dipalmitin, cholesterol isocaproate, cholest-5-ene, 3-(1-oxobuthoxy)-, cholesta-3,5-diene. CONCLUSION: These results suggest the cardioprotective potential of ferulic acid against diabetic cardiomyopathy.