Restoration of renal hemodynamics and functions by administration in dinitrophenol-induced hypoxia in rat's animal model.

Objective: Hypoxia is one of the principal causes of renal diseases. This study aimed to evaluate the effects of on dinitrophenol (DNP)-induced hypoxia renal damage in rats.

Methods: Forty adult male rats were incorporated in this study. The rats were divided into four groups: control group, group, DNP hypoxic group, and DNP + group receiving (400 mg/kg body weight). Serum and renal tissue erythropoietin (EPO) hormone and hypoxia-inducible factor-2α (HIF-2α) levels were measured. Renal oxidative stress biomarkers, inflammatory biomarkers, renal hemodynamics, and histopathological examination were evaluated.

Results: Administration of highly significantly normalized serum EPO level, HIF-2α ( < 0.001 for each) in DNP + treated rats as compared to DNP hypoxic rats. Furthermore, it highly significantly improved renal oxidative stress evident by decreased renal tissues malondialdehyde and increased superoxide dismutase, total thiol, and catalase activity ( < 0.001 for each). Furthermore, a highly significant decline of renal intercellular adhesion molecule-1, myeloperoxidase, and interleukin-6 was observed in DNP + rats ( < 0.001 for each). Improvements in renal hemodynamics and kidney functions were also found after administration (with < 0.001 for all parameters). In addition, treatment reduced renal histopathological changes of the DNP + group. Our results were statistically analyzed using the Prism software package (GraphPad version 8.0).

Conclusion: has an alleviating effect on DNP-induced hypoxia renal damage and can restore kidney functions in rats' animal models. These effects were through antioxidant, anti-inflammatory, and hemodynamic mechanisms.