Renoprotective and antioxidative effects of methanolic Paederia foetida leaf extract on experimental diabetic...

Paederia foetida Linn. (Family: Rubiaceae) is widely used as a natural remedy for diabetes mellitus by the Nepali and Lepcha tribes of Sikkim and Darjeeling Himalayan region. The plant is administered to a diabetic individual in the form of leaf infusion for 2-3 weeks. Therefore, we investigated the effects of methanolic leaf extract of Paederia foetida (MEPF) on alloxan (ALX) induced diabetic renal oxidative stress and NF-kB dependent renoinflammatory events in rat. Method Effects of MEPF on blood glucose, glomerular filtration rate (GFR), serum and oxidative stress markers were evaluated in ALX induced diabetic wistar rats. Enzyme linked immunosorbent assay (ELISA) was carried out to estimate serum IL-6, IL-1β, TNF-α and renal tissue NF-kB p65 levels. MEPF treatment was given to the diabetic rats at a dose of 250 and 500mg/kg body weight (b.w.).

MEPF treatment significantly reduced hyperglycaemia, serum creatinine, blood urea nitrogen (BUN), bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglycerides (TRIGs), and total cholesterol (TCHOL) levels in the diabetic rats, whereas it significantly restored GFR and serum albumin level. The activity of enzymatic and non-enzymatic antioxidant machineries was remarkably augmented by MEPF treatment. Likewise, it also significantly lowered lipid peroxidation which was evidenced by decreased concentration of thiobarbituric reactive substances (malondialdehyde, MDA) in the renal tissue of treated diabetic groups. Moreover, MEPF treated animals exhibited low serum concentrations of IL-6, IL-1β and TNF-α compared to the diabetic control rats. It showed a dose dependent inhibition of NF-kB activation in the diabetic kidney, but the effects were more prominent at a dose of 500mg/kg. Histopathological examinations also confirmed its nephroprotective action during diabetes.

MEPF treatment mitigates oxidative stress and suppresses renal inflammation via inhibition of NF-kB in diabetic kidney in early progressive diabetic nephropathy.