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    Aesculus hippocastanum Alleviates Diabetic Neuropathy by Reducing MMP-9 and MMP-10 Levels
    (Asian Network Scientific Information-Ansinet, 2023) Gonullu, Edip; Dagistan, Gozde; Ozsezer, Yakup; Erdogan, Mumin Alper; Erbas, Oytun
    Background and Objective: Diabetic neuropathy (DN) is a prevalent complication of diabetes, characterized by neuropathic pain and motor dysfunction. The role of oxidative stress and inflammation in DN pathophysiology is well-documented. This study aims to evaluate the therapeutic potential of Aesculus hippocastanum (AH) in mitigating DN symptoms, focusing on its antioxidant and anti-inflammatory properties. Materials and Methods: The study utilized 40 adult male Wistar rats, divided into four groups: Control, diabetic and two AH-treated groups (receiving 10 mg kgG1 and 20 mg kgG1 AH, respectively). Diabetes was induced using streptozotocin (STZ) injections. Evaluations included lipid peroxidation (via malondialdehyde levels), matrix metalloproteinases (MMP-9 and MMP-10) levels, electrophysiological records (assessing compound muscle action potential), histopathological examination of the sciatic nerve and motor function tests (using an inclined plane). Results: The AH-treated groups exhibited a significant reduction in MDA levels, indicating decreased lipid peroxidation. Plasma MMP-9 and MMP-10 levels were also lower in these groups, suggesting reduced inflammation. Electrophysiological records showed increased CMAP amplitudes and decreased distal latency in AH-treated rats, indicative of improved nerve conduction. Histopathological examination revealed reduced perineural thickness in the sciatic nerve of AH-treated rats, suggesting less fibrosis. In motor function tests, AH-treated rats demonstrated enhanced performance, implying improved muscle strength and motor capacity. Conclusion: The findings indicate that AH treatment effectively reduces oxidative stress and inflammation in a rat model of diabetic neuropathy, leading to improved neuropathic symptoms. These results suggest that AH could be a promising therapeutic agent for managing DN, warranting further investigation for its potential clinical application.
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    Demonstration of the protective effect of propofol in rat model of cisplatin-induced neuropathy
    (Aepress Sro, 2023) Gonullu, Edip; Dagistan, Gozde; Erkin, Yuksel; Erdogan, Mumin Alper; Erbas, Oytun
    Cisplatin is commonly used in the treatment of lung, genitourinary, and gastrointestinal cancers. Peripheral neuropathy is the most important side effect, leading to a decrease in the dose of cisplatin or its complete cessation in the early period. 16 rats were given cisplatin at a dose of 2.5 mg/ kg/day twice a week for 4 weeks to induce neuropathy model. The rats taking Cisplatin were divided into 2 groups. Group 1 rats (n = 8) were given 1 ml/kg/day 0.9 % NaCl intraperitoneally, and Group 2 rats were given 10 mg/kg/day Propofol intraperitoneally daily for 4 weeks. The remaining 8 rats served as the control group. At the end of the study, all animals were tested for motor functions. Blood samples were collected for the measurement of plasma lipid peroxidation (malondialdehyde; MDA), tumor necrosis factor (TNF-alpha), glutathione (GSH), IL-6 and HSP-70 levels. Electromyography findings revealed that compound muscle action potential (CMAP) amplitude was significantly higher in the cisplatin-Propofol group than in the cisplatin-saline group. Also, cisplatin-Propofol treated group showed significantly lower TNF-alpha, MDA and IL-6 levels and higher GSH and HSP-70 levels than cispalatin-Saline group (p < 0.01, p < 0.001). In addition, while the CMAP latency was decreased in the propofol group, the CMAP amplitude was increased, and a significant improvement was observed in the Inclined test scores. Besides, histological examinations showed an increase in axon diameter and NGF expression with Propofol treatment. This study demonstrated that Propofol exerts protective activity against cisplatin-induced neurotoxicity by increasing endogenous antioxidants and reducing lipid peroxidation and inflammation (Tab. 3, Fig. 4, Ref. 30). Text in PDF www.elis.sk