Visnagin Attenuates Gestational Diabetes Mellitus in Streptozotocin-induced Diabetic Pregnant Rats via Regulating Dyslipidemia, Oxidative Stress, and Inflammatory Response

ABSTRACT

Background: Gestational diabetes mellitus (GDM) is a condition of glucose intolerance and insulin resistance only diagnosed during pregnancy. GDM has exhibited several adverse effects on both mother and offspring. The current research focuses on discovering visnagin’s beneficial properties against the streptozotocin (STZ)-induced GDM in rats via alleviating the inflammation and oxidative stress. Materials and Methods: GDM was caused in the pregnant rats by the administration of 25 mg/kg of STZ by the intraperitoneal route and then treated with 20 mg/kg of visnagin for 20 consecutive days. The rats’ body weight was measured, and fasting blood glucose (FBG) status was determined using a standard glucometer. The contents of total cholesterol (TCh), triglycerides (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were assessed using kits. The MDA level, total antioxidant capacity (TAC) status, and activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST) were determined using assay kits. Kits also assessed the contents of TNF-α and IL-1β. The contents of TNF-α and IL-1β effectively improved the body weight and decreased the FBG status in the GDM rats. The visnagin also decreased the TCh, TG, and LDL, and elevated the HDL content. The content of MDA was decreased and the visnagin treatment increased SOD, CAT, GST, and GPx, and the visnagin treatment increased SOD, CAT, GST, and GPx activities SOD, CAT, GST, and GPx activities. The visnagin effectively decreased the STZ-induced histopathological alterations in the pancreas. Conclusion: Altogether, our investigation results suggest a beneficial role visnagin against STZ-induced GDM in rats via inhibiting the inflammatory responses. Hence, it can be a talented therapeutic candidate for the successful management of GDM.

KEYWORDS

• Insulin resistance
• dyslipidemia
• glucose intolerance
• visnagin

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• DOI10.1177/09731296221137440Copy

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