Visnagin Mitigates Glycerol-induced Acute Kidney Injury in Rats through Decreasing Inflammation, Oxidative Stress, and Renal Dysfunction Markers

Background: Acute kidney injury (AKI) is a heterogenous condition, characterized by dysregulated kidney function along with reduced glomerular filtration, solute excretion, and urine output. Objectives: This work was focused to investigate the therapeutic roles of visnagin against the glycerol-induced AKI in rats via reducing the inflammation and oxidative stress responses. Materials and Methods: The AKI was induced in the Wistar rats by injecting 50% of glycerol (10 ml/kg). Then AKI rats were treated with 20 and 40 mg/kg of visnagin, respectively for 12 consecutive days. The rats were sacrificed followed at the end of experiments and blood and renal tissue samples were collected. The creatinine, BUN, urea, and LDH was quantified using assay kits. The nitric oxide (NO), MDA, and MPO were analyzed using assay kits. The antioxidants such as GSH, SOD, GSH, GPx, GR, and CAT activities were assessed by the standard methods. The IL-1β, IL-6, TNF-α, TGF-β1, MCP-1, and ICAM-1 levels were measured using assay kits. The histopathological analysis was done on the renal tissues. Results: The 20 and 40 mg/kg of visnagin treatment reduced the relative kidney weight of AKI rats. The urea, creatinine, BUN, and LDH levels were diminished by the visnagin. The 20 and 40 mg/kg of visnagin treated AKI rats appreciably reduced the MDA, MPO, and NO levels and augmented the GSH, SOD, GPx, GR, and CAT activities in the renal tissues. The IL-6, IL-1β, TNF-α, and TGF-1β levels were reduced by the visnagin treatment. The MCP-1 and ICAM-1 status were also diminished by the visnagin. The findings of the histopathological analysis revealed that visnagin attenuated the glycerol-induced AKI in rats. Conclusion: In conclusion, the outcomes of this study revealed that the visnagin demonstrated nephroprotective effects against glycerol-induced renal damage in rats. The ability of visnagin to ameliorate inflammatory response, oxidative stress, and renal dysfunction make it a potential candidate for treating AKI.