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    Extremely low-frequency pulsed electromagnetic fields induce apoptotic, oxidative stress, inflammatory and aquaporin-related kidney alteration
    (Springer, 2026) Pekince Ozoner, Merve; Seker, Ugur; Sert, Cemil; Tuysuz, Mehmet Zahid; Yuksel, Meral; Gokce, Yasin
    Extremely low-frequency pulsed electromagnetic fields are used as a biotherapy method in various medical and experimental applications. However, the cellular effects of prolonged or intense exposure remain unclear. This study aimed to evaluate the effects of two different ELF-PEMF doses on kidney tissue over an 8 week period, investigating oxidative stress, apoptosis, inflammation, and aquaporin expression using biochemical, histopathological, and immunohistochemical methods. Forty male rats were assigned to control, sham, 1 mT, and 5 mT groups; the 1 mT and 5 mT groups were exposed to ELF-PEMF for four hours daily for eight weeks, while controls received no intervention. At the end of the experiment, kidney tissues were collected for histopathological (H&E and PAS), immunohistochemical and biochemical analyses. In kidney tissue exposed to ELF-PEMF, hyperemia, tubular degeneration, and proteinaceous casts were observed. 1 mT and 5 mT ELF-PEMF exposure increased BAX, Caspase-9, and TNF-alpha immunoreactivity compared to the control and sham groups, while no change was observed in BCL-2 expression. 5 mT group exposure to ELF-PEMF increased AQP3 expression, a critical water channel in cellular H2O2 permeability (p < 0.05). AQP5 expression was significantly increased in both the 1 mT and 5 mT groups compared to the control group (p < 0.05). Biochemical analyses showed that oxidative stress levels were significantly increased in both the 1 mT and 5 mT groups compared to the control group (p < 0.05). These findings suggest that, despite its recent use for its therapeutic properties, long-term exposure to ELF-PEMF may cause oxidative stress, apoptosis, and inflammation in renal tissue and alter the histological structure and cellular homeostasis. [GRAPHICS] .
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    Nephroprotective effects of visnagin through modulation of macrophage polarization, oxidative stress, inflammation and apoptosis in renal I/R injury
    (De Gruyter Poland Sp Z O O, 2026) Sagir, Suleyman; Seker, Ugur; Pekince-Ozoner, Merve; Yuksel, Meral; Gokdemir, Gul Sahika; Kaya, Seval; Demir, Mehmet
    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, Visnagin30 mg/kg, Visnagin60 mg/kg, I/R, I/R + Visnagin30 mg/kg, I/R + Visnagin60 mg/kg (n=7). Bilateral renal ischemia was induced by clamping for 25 min, followed by 2 h of reperfusion. Visnagin or vehicle was administered to the animals intraperitoneally 2 h 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-1 beta, 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 60 mg/kg significantly reduced MDA, CL, and IL-1 beta levels, and increased GSH (p<0.05). Immunohistochemically, visnagin decreased Bax (p<0.001), caspase-3 (p<0.01), and TNF-alpha (p<0.01) expressions elevated by I/R injury. Furthermore, visnagin reversed I/R induced M1/M2 macrophage polarization (CD86 up arrow, CD163 down arrow), decreasing CD86 (p<0.05) and increasing CD163 immunodensity (p<0.05). Conclusions: Visnagin treatment (60 mg/kg) exerts promising nephroprotective effects in renal I/R injury by reducing oxidative stress, inflammation, apoptosis, and modulating M1/M2 macrophage polarization.
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    Öğe
    Regulation of STAT3 and NF-κB signaling pathways by trans-Anethole in testicular ischemia-reperfusion injury and its gonadoprotective effect
    (MRE Press, 2024) Seker, Ugur; Gökçe, Yasin; Kati, Bulent; Yuksel, Meral; Guzel, Baris Can; Shokoohi, Majid
    Testicular ischemia reperfusion (I/R) injury is a significant urological problem where clinical interventions may be inadequate, and the antioxidants might be potential co-treatment modalities. This study examined the gonadoprotective effect of trans-Anethole in testicular I/R injury. Twenty-eight male rats were divided into four groups. Rats in the I/R, I/R + t100, I/R + t200 groups underwent bilateral testicular I/R injury. The I/R + t100 and I/R + t200 groups received 100 or 200 mg/kg trans-Anethole at the 2nd hour of ischemia. Microscopic evaluations demonstrated that testicular I/R injury leads to severe testicular degeneration. Tissue oxidative stress, pro-apoptotic Bcl-2 associated X (Bax) and Caspase 3, pro-inflammatory Tumor necrosis factor-alpha (TNF-?), Interleukin-1 beta (IL-1?) and Interleukin 6 (IL-6) cytokines levels were significantly (p < 0.05) upregulated when compared to the Control group. Additionally, transcription factors Signal transducer and activator of transcription 3 (STAT3) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-?B) levels increased significantly (p < 0.05) compared to the Control group. Tissue disrupted parameters in the I/R + t200 group were significantly different (p < 0.05) from the I/R group, contrasting with the slight improvement in the I/R + t100 group. The STAT3 and NF-?B expression levels in the I/R + t200 group were significantly suppressed (p < 0.05) compared to the I/R group. In conclusion, our study indicates that trans-Anethole could enhance gonadoprotective activity in testicular I/R injury, potentially involving transcription factors STAT3 and NF-?B. However, before the consumption of trans-Anethole-containing natural or manufactured goods, the potential benefits and side effects should be carefully evaluated. © 2024 The Author(s).