Akademik Veri Yönetim Sistemi
Open Medicine (Poland), cilt.21, sa.1, 2026 (SCI-Expanded, Scopus)
Objectives: The study aimed to investigate the nephroprotective effects of visnagin on renal ischemia-reperfusion (I/R) injury and the role of M1/M2 macrophage polarization in this process. Methods: Forty-two adult rats were divided into six groups: Control, Visnagin30mg/kg, Visnagin60mg/kg, I/R, I/R + Visnagin30mg/kg, I/R + Visnagin60mg/kg (n=7). Bilateral renal ischemia was induced by clamping for 25min, followed by 2h of reperfusion. Visnagin or vehicle was administered to the animals intraperitoneally 2h before reperfusion. At the end of the study, kidney samples were collected for analysis of oxidative stress, inflammatory cytokines, apoptotic protein expression, and M1/M2 macrophage polarization. Results: I/R injury increased malondialdehyde (MDA), chemiluminescence (CL), IL-1β, and IL-6 levels while decreasing glutathione (GSH) in renal tissue, indicating enhanced oxidative stress (p<0.001) and inflammation (p<0.05). Histopathological examination showed glomerular atrophy, tubular degeneration, and intertubular hemorrhage. Visnagin treatment at 60mg/kg significantly reduced MDA, CL, and IL-1β levels, and increased GSH (p<0.05). Immunohistochemically, visnagin decreased Bax (p<0.001), caspase-3 (p<0.01), and TNF-α (p<0.01) expressions elevated by I/R injury. Furthermore, visnagin reversed I/R induced M1/M2 macrophage polarization (CD86↑, CD163↓), decreasing CD86 (p<0.05) and increasing CD163 immunodensity (p<0.05). Conclusions: Visnagin treatment (60mg/kg) exerts promising nephroprotective effects in renal I/R injury by reducing oxidative stress, inflammation, apoptosis, and modulating M1/M2 macrophage polarization.