Department of Anesthesiology and Reanimation, Izmir Katip Celebi University Ataturk Training and Research Hospital, Izmir 35000, Türkiye.
Department of Physiology, Faculty of Medicine, Izmir Katip Celebi University, Izmir 35000, Türkiye.
Medicina (Kaunas). 2024 Sep 26;60(10):1580. doi: 10.3390/medicina60101580.
: This study aimed to investigate the protective effect of diosmin and hesperidin in diabetic neuropathy using a rat model, focusing on their impact on nerve regeneration through the fibroblast growth factor 21 (FGF21) and galectin-3 (gal3) pathway. Forty adult male Wistar rats were used in this study. Diabetes was induced using streptozotocin (STZ), and the rats were divided into control, diabetes and saline-treated, diabetes and diosmin + hesperidin (150 mg/kg) treated, and diabetes and diosmin + hesperidin (300 mg/kg) treated groups. Electromyography (EMG) and inclined plane testing were performed to assess nerve function and motor performance. Sciatic nerve sections were examined histopathologically. Plasma levels of FGF21, galectin-3, and malondialdehyde (MDA) were measured as markers of oxidative stress and inflammation. Diabetic rats treated with saline displayed reduced nerve conduction parameters and impaired motor performance compared to controls. Treatment with diosmin and hesperidin significantly improved compound muscle action potential (CMAP) amplitude, distal latency, and motor performance in a dose-dependent manner. Histopathological examination revealed decreased perineural thickness in treated groups. Additionally, treatment with diosmin and hesperidin resulted in increased plasma FGF21 levels and reduced plasma levels of galectin-3 and MDA, indicating decreased oxidative stress and inflammation. Diosmin and hesperidin exhibited protective effects in diabetic neuropathy by promoting nerve regeneration, enhancing nerve conduction, and improving motor performance. These effects were associated with modulation of the FGF21 and galectin-3 pathway. These findings suggest that diosmin and hesperidin may hold potential as adjunctive therapies for diabetic neuropathy.
本研究旨在通过大鼠模型探究地奥司明和橙皮苷对糖尿病神经病变的保护作用，重点关注它们通过成纤维细胞生长因子 21（FGF21）和半乳糖凝集素-3（gal3）通路对神经再生的影响。本研究使用了 40 只成年雄性 Wistar 大鼠。采用链脲佐菌素（STZ）诱导糖尿病，将大鼠分为对照组、糖尿病和盐水治疗组、糖尿病和地奥司明+橙皮苷（150mg/kg）治疗组、糖尿病和地奥司明+橙皮苷（300mg/kg）治疗组。通过肌电图（EMG）和斜面试验评估神经功能和运动表现。对坐骨神经切片进行组织病理学检查。测量血浆中 FGF21、半乳糖凝集素-3 和丙二醛（MDA）的水平，作为氧化应激和炎症的标志物。与对照组相比，糖尿病和盐水治疗组的大鼠表现出神经传导参数降低和运动表现受损。地奥司明和橙皮苷治疗以剂量依赖的方式显著改善了复合肌肉动作电位（CMAP）幅度、远端潜伏期和运动表现。组织病理学检查显示，治疗组的神经周围厚度减小。此外，地奥司明和橙皮苷治疗导致血浆 FGF21 水平升高，血浆 galectin-3 和 MDA 水平降低，表明氧化应激和炎症减轻。地奥司明和橙皮苷通过促进神经再生、增强神经传导和改善运动表现，对糖尿病神经病变具有保护作用。这些作用与 FGF21 和 gal3 通路的调节有关。这些发现表明，地奥司明和橙皮苷可能作为糖尿病神经病变的辅助治疗方法具有潜力。
