Momordica charantia polysaccharides mitigate the progression of STZ induced diabetic nephropathy in rats

• Protective effect of Momordica charantia polysaccharides (MCP) treatment on of STZ-induced DN in rats.
• MCP reduces oxidative stress via antioxidant redox signaling pathway.
• MCP restored the antioxidant ability by down regulating lipid peroxidation (MDA) and up regulating antioxidant enzymes.
• MCP mitigates the progression of DN in rats through suppression of oxidative stress and modulation of the Nrf2 and HO-1 pathway.
• MCP mitigates the magnitude of histologic renal damage to diabetic rats.

Diabetic nephropathy (DN) has become a primary cause of end-stage kidney disease. Several complex dynamics converge together to accelerate the advancement of DN. The present investigation was postulated to explore the mechanism of reno-protective nature of Momordica Charantia polysaccharides (MCP) by evaluating the anti-hyperglycemic, anti-lipidemic as well as markers for oxidative stress and antioxidant proficiency in streptozotocin (STZ)-induced diabetic rats. The oral administration of MCP showed a significant normalization in the levels of kidney function test in the STZ-induced diabetic rats. The levels of blood urea nitrogen (BUN), urea protein and creatinine increased by 316.58%, 195.14% and 800.97% respectively, in STZ-induced diabetic rats when compared with normal rats. MCP treatment also illustrated a significant improvement in glutathione peroxidase, superoxide dismutase and catalase levels, with a significant decline in MDA in diabetic kidneys. Immunoblots of heme-oxygenase 1 (HO-1) and Nrf2 of MCP treated diabetic rats showed a significant up-regulation of HO-1 and Nrf2 protein. Histological and ultra-structural observations also reveal that MCP efficiently protects the kidneys from hyperglycemia-mediated oxidative damage. These findings illustrate that the reno-protective nature of MCP mitigates the progression of STZ induced DN in rats by suppression of oxidative stress and amelioration of the HO-1/Nrf2 pathway.