Investigating the role of polyphenols from Pleurospermum candollei (DC.) extract against diabetic nephropathy through modulating inflammatory cytokines and renal gene expression in rats.

• Pleurospermum candollei possess high inhibition activity against DPPH radicals and alpha glucosidase enzyme. • P. candollei can reduce the diabetic effects of streptozotocin. • P. candollei can normalize the production of antioxidant enzymes and free radicals in rat kidney. • P. candollei can regulate the inhibition of inflammatory, and apoptotic mediators. • P. candollei can be used as potent drug against diabetes induced nephropathy. Pleurosepermum candollei is a local vegetable that is traditionally used to cure abdominal problems, pain, and infertility. The purpose of this study was to evaluate the therapeutic potential of P. candollei ethanolic extract against T2DM through modulation of renal genetic markers. Biochemical composition of extract was investigated through high performance liquid chromatography and quantitative phytochemical analyses. In rats, T2DM was induced by injecting streptozotocin (STZ), and P. candollei ethanol extract was administered for 21 days. Antioxidant enzymes and renal biomarkers were assessed in homogenized kidney samples of treated groups. qRT-PCR analysis of isolated RNA was performed for estimation of inflammatory and apoptotic markers. These biochemical analyses revealed that plant extract significantly normalized the levels of catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) after 21 days of treatment. However, high dose of plant extract (300 mg/kg) exhibited more prominent results in restoring the inflammatory (IL-6, IL-β1, and TNF-α) and apoptotic markers than low dose (150 mg/kg). Similarly, histological studies also revealed that there was minor inflammation and necrosis in kidney of plant treated rats. Generally, the present study showed that administration of P. candollei extract exhibits renal protective, anti-hyperglycemic, and anti-glycation properties. However, further research is required to assess the mechanism of action of PCE at clinical level. [Display omitted] [ABSTRACT FROM AUTHOR]