PROTECTIVE EFFECT OF EPROSARTAN IN RENAL ISCHEMIA REPERFUSION INJURY BY REGULATING OXIDATIVE STRESS, INFLAMMATION, AND APOPTOTIC CASCADES IN A BILATERAL RAT MODEL.

OBJECTIVE: The aim: To evaluate the potential protective effect of Eprosartan (ARB) in bilateral renal IRI in male rats. PATIENTS AND METHODS: Materials and methods: 20 Sprague-Dawley rats divided into four groups. Sham group had surgery without IRI. Control group was subjected to 30 min ischemia and 2 hours of reperfusion. Vehicle group received 14 ml/kg (IP) injection of solvent mixture containing (10% DMSO, 40% PEG300, 5% Tween-80, and 45% normal saline) 30 minutes before clamping. Eprosartan-treated group with 30 mg/kg Eprosartan intraperitoneally 30 min before occlusion of renal pedicles followed by 30 minutes of ischemia and 2 hours of reperfusion. Serum BUN and Creatinine used to assess renal function. Renal tissue was used to measure the levels of TNF-α, IL-1ß, IL-6, F2-isoprostane, and Caspase3 were measured by assessment of renal tissue. Histopathological examinations were conducted to detect parenchymal damage. RESULTS: Results: Mean serum levels of BUN and Creatinine as well as mean renal tissue levels of TNF-α, IL-1ß, IL-6, F2-isoprostane, and Caspase3 were significantly increased in control and vehicle groups together with increase in histological damage score compared to sham group, whereas treatment of rats with Eprosartan resulted in significant reduction in mean serum levels of BUN and Creatinine and mean renal tissue levels of TNF-α, IL-1ß, IL-6, F2-isoprostane, and Caspase3 and obvious reduction in tissue injury. CONCLUSION: Conclusions: This study demonstrates that Eprosartan pretreatment enhances kidney function by decreasing serum BUN and Creatinine, oxidative stress, cytokines, and apoptotic markers.

Cardamonin mitigates kidney injury by modulating inflammation, oxidative stress, and apoptotic signaling in rats subjected to renal ischemia and reperfusion.

Renal ischemia-reperfusion injury (IRI) is a critical health concern that aggravates the pathophysiology of acute kidney injury (AKI), leading to high mortality rates in intensive care units. Cardamonin is a natural compound with anti-inflammatory and antioxidant properties. The current study aimed to evaluate the renoprotective impact of cardamonin against AKI induced by renal IRI. Male rats (n=5 per group) were divided into four groups: the sham group underwent anesthesia and abdominal incision only; the control group experienced bilateral renal artery clamping for 30 minutes followed by 2 hours of reperfusion; the vehicle group received the cardamonin vehicle 30 minutes before ischemia induction; and the cardamonin group was administered 5 mg/kg of cardamonin 30 minutes before ischemia. Blood urea nitrogen (BUN) and creatinine were measured to assess the renal function. Tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß), interleukin-6 (IL-6), caspase 3, and F2-isoprostane were assessed in renal tissues. Kidney injury was examined using the hematoxylin and eosin stain method. Compared to the sham group, the control group exhibited significantly higher levels of BUN, creatinine, TNF-α, IL-1ß, IL-6, F2-isoprostane, and caspase 3 in renal tissues, along with severe kidney injury as evidenced by histological analysis. Compared to the control group, pretreatment with cardamonin resulted in a significant reduction in these biomarkers and alleviated renal damage. Cardamonin had renoprotective effects against renal ischemia and reperfusion injury via modulating inflammation, oxidative stress, and apoptosis pathways.