ArticleBMC nephrology2025
Adropin as a protective agent against renal ischemia-reperfusion injury induced by suprarenal aortic cross-clamping in rats.
Article in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe development of protective therapeutic strategies against acute kidney injury associated with suprarenal aneurysms, renal artery occlusive disease, and suprarenal aortic reconstruction is of paramount importance. Adropin is a peptide hormone that has been shown to protect vascular endothelial cells and reduce oxidative stress, apoptosis, and inflammation. Therefore, in addition to its metabolic and vascular effects, adropin has potential as a therapeutic agent in renal ischemia-reperfusion injury. This study aims to investigate the protective effects of adropine on kidney ischemia-reperfusion (IR) injury under the suprarenal aortic cross clamp.
methodsMale Sprague Dawley rats were divided into six groups, with seven rats in each group for the study design. The control and ischemia reperfusion (IR) induced groups were designated as the two groups while the other four groups (TR1 to TR4 ) were administered varying doses of adropin at 0.5 mg/kg, 1 mg/kg, 1.5 mg/kg, and 2 mg/kg for each group. After a 60 min ischemic period, a 24-hour reperfusion period was implemented to assess the outcomes of adropin treatment on renal IR. Histopathological analysis was performed in conjunction with determination of apoptosis, and malondialdehyde (MDA) levels. In addition, serum concentrations of adropin, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), as well as endothelial nitric oxide synthase (eNOS) were measured in order to further define the biochemical reactions of the treatment.
resultsMDA levels were significantly elevated in the IR group compared to the control group, while the activities of eNOS, SOD, and GSH-Px enzymes were significantly decreased (P < 0.05). MDA levels in the treatment groups were lower than those in the IR group, whereas eNOS, SOD, and GSH-Px levels were higher (P < 0.05). Statistically, the lowest adropin levels were observed in the IR group, while the highest levels were noted in the TR4 group (P < 0.05). Histopathological examination revealed a reduction in tissue damage in the treatment groups compared to the IR group.
conclusionThe histological and biochemical findings from this study indicate that adropin provides protective effects against renal ischemia-reperfusion injury in a dose-dependent manner.
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