Aim Background: Ischemia/reperfusion renal injury (IRI), which is predominantly brought on by inflammation and oxidative stress, is the main cause of acute kidney damage. Aims: This work uses a male Wistar Albino rat model of experimentally induced renal ischemia-reperfusion injury (IRI) to examine the nephroprotective potential of Urolithin A. Material and methods Materials and methods: Twenty-eight rats (N=7) were randomly assigned to four groups: DMSO pre-injection as a vehicle, bilateral renal IRI for 30 minutes followed by two hours of reperfusion as a control, sham (laparotomy without IRI), and treatment (Urolithin A pre-injection for three days). ELISA and histological analysis were used to assess biomarkers of kidney injury, oxidative stress, inflammation, and apoptosis. Results Results: While GSH levels were enhanced, Urolithin A therapy primarily decreased TNF-α, IL-1β, MDA, Caspase-3, and KIM-1 levels. Furthermore, the group treated with Urolithin A showed a substantial downregulation of FOXO3 expression. Histopathological results verified that the therapy group had less kidney damage. Conclusions Conclusion: These findings suggest that Urolithin A produces nephroprotective effects against IRI via modulating oxidative stress, inflammation, and apoptosis, particularly through the control of FOXO3. This study suggests that Urolithin A is a good treatment candidate for renal IRI control.
Abosaooda et al. (Tue,) studied this question.