Nesfatin-1 peptide protects rat renal epithelial cells against high glucose and H₂O₂ induced injury via inhibition of oxidative stress, apoptosis, and fibrosis

Nesfatin-1 is a potent polypeptide and plays a crucial role in many physiological functions. Nesfatin-1 levels are reported in both the central nervous system and peripheral organs. However, the expression of nesfatin-1 in the renal system under chronic oxidative stress-induced conditions and the direct effect of nesfatin-1 treatment on stress-induced pathological damage are not reported. Thus, the present study aimed to explore the role of nesfatin-1 in vitro in oxidative stress-induced renal epithelial cells. High glucose (HG) and H₂O₂ combination were used to induce oxidative stress (OS). MTT, crystal violet, and H and E staining were used to measure cell viability, cytotoxicity, and morphology. FACS analysis and confocal microscopy were used to measure OS and apoptosis. RT-PCR was done for gene expression analysis. Decreased nesfatin-1 expression was observed in renal epithelial cells induced with HG and H₂O₂ compared to an untreated control (0.16; p < 0.0001). Nesfatin-1 co-treatment with HG and H₂O₂ attenuated ROS, apoptosis, and fibrosis. SOD, Catalase, and Bcl-2 expression decreased (p < 0.0001) and Caspase-3 and TGF-β1 expression increased in HG and H₂O₂-induced cells compared to control cells (p < 0.0001). Nesfatin-1 co-treatment attenuated these changes induced by HG and H₂O₂ (p < 0.0001). Nesfatin-1 expression was decreased in renal epithelial cells under stress-induced conditions. Moreover, nesfatin-1 co-treatment under stress-induced conditions protects the renal epithelial cells via inhibition of oxidative stress, apoptotic, and fibrotic signaling pathways.