Effect of madecassoside in reducing oxidative stress and blood glucose in streptozotocin–nicotinamide-induced diabetes in rats

Abstract

Objectives Madecassoside (MAD) is a triterpenoid constituent of Centella asiatica (L.) Urb., an ethnomedical tropical plant, extracts of which were shown to reduce blood glucose in experimental diabetes. This study examines MAD for its anti-hyperglycaemic effects and tests the hypothesis that it reduces the blood glucose in experimentally induced diabetic rats by protecting the β-cells. Methods Diabetes was induced using streptozotocin (60 mg/kg, i.v.) followed by nicotinamide (210 mg/kg, intraperitoneal (i.p.)). MAD (50 mg/kg) was administered orally for 4 weeks, commencing 15 days after induction of diabetes; resveratrol (10 mg/kg) was used as a positive control. Fasting blood glucose, plasma insulin, HbA1c, liver and lipid parameters were measured, along with antioxidant enzymes and malondialdehyde as an index of lipid peroxidation; histological and immunohistochemical studies were also undertaken. Key findings MAD normalized the elevated fasting blood glucose levels. This was associated with increased plasma insulin concentrations. MAD alleviated oxidative stress by improving enzymatic antioxidants and reducing lipid peroxidation. Histopathological examination showed significant recovery of islet structural degeneration and an increased area of islets. Immunohistochemical staining showed increased insulin content in islets of MAD-treated rats. Conclusions The results demonstrate an antidiabetic effect of MAD associated with preservation of β-cell structure and function.

Curculigoside mitigates dextran sulfate sodium‑induced colitis by activation of KEAP1‑NRF2 interaction to inhibit oxidative damage and autophagy of intestinal epithelium barrier

“…In the present study, downregulation of levels of SOD, CAT and GSH suggested that the activity of the antioxidant enzyme system induced by bowel inflammation was suppressed, whereas this trend was reversed upon administering CUR, indicating recovery of the activity of the antioxidant enzyme defense system. In addition, MAD is a lipid peroxidation metabolite commonly used as a marker to measure lipid peroxidation metabolism in vivo , serving as an indicator to assess the generation of free radicals and damage they cause to the structure of the membrane lipid bilayer ( 47 ). In the present study, downregulation of MAD following CUR administration demonstrated elimination of oxidative stress mediated by CUR that occurred during inflammation.…”