Crocin Improves Diabetes-Induced Oxidative Stress via Downregulating the Nox-4 in Myocardium of Diabetic Rats

Oxidative stress has a crucial role in the pathophysiology of cardiac dysfunction in the diabetic milieu. Crocin is a natural compound that acts as an antioxidant which could potentially ameliorate oxidative damages in various tissues. The potential role of crocin in the myocardial tissue is not clear yet. This study was aimed to evaluate the possible antioxidative properties of crocin in the myocardium of diabetic rats.

Male Wistar rats were randomly divided into four groups as normal, normal-treated, diabetic, and diabetic-treated. Diabetes was induced by a single intravenous injection of STZ (40 mg/kg). Two treated groups of animals (diabetic and non-diabetic) were treated with crocin daily for 8 weeks (40 mg/kg/IP). At the end of day 56, animals were sacrificed under deep anesthesia, and blood and tissue samples were collected. After tissue preparation, the level of nitrate, malondialdehyde, and glutathione and the activity of superoxide dismutase and catalase enzymes were measured via standard protocols. In addition, the level of Nox-4 mRNA expression was examined by RT-PCR method. The data were analyzed via one-way ANOVA, and P < 0.05 was considered as a significant difference.

Diabetes induces oxidative damages by upregulating the Nox-4 enzyme and increasing nitrate and malondialdehyde levels in the myocardium. Diabetes reduced the superoxide dismutase, catalase, and glutathione activities in the myocardial tissues. Treatment with crocin reversed these changes, reduced Nox-4 mRNA expression, and reduced the nitrate and malondialdehyde content in the myocardium of diabetic rats.

Diabetes induces oxidative stress in myocardium via the upregulating Nox-4 enzyme, and the treatment with crocin reversed these changes. Thus, crocin could be considered as a novel agent for potentially protecting myocardial tissues against diabetes-induced oxidative damages.