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(-)-Epigallocatechin gallate attenuates NADPH-dNOS expression in motor neurons of rats following peripheral nerve injury

机译:(-)-表没食子儿茶素没食子酸酯减弱周围神经损伤后大鼠运动神经元中NADPH-d / nNOS的表达

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摘要

BackgroundOxidative stress and large amounts of nitric oxide (NO) have been implicated in the pathophysiology of neuronal injury and neurodegenerative disease. Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has potent antioxidant effects against free radical-mediated lipid peroxidation in ischemia-induced neuronal damage. The purpose of this study was to examine whether EGCG would attenuate neuronal expression of NADPH-dNOS in the motor neurons of the lower brainstem following peripheral nerve crush. Thus, young adult rats were treated with EGCG (10, 25, or 50 mg/kg, i.p.) 30 min prior to crushing their hypoglossal and vagus nerves for 30 seconds (left side, at the cervical level). The treatment (pre-crush doses of EGCG) was continued from day 1 to day 6, and the animals were sacrificed on days 3, 7, 14 and 28. Nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were used to assess neuronal NADPH-dNOS expression in the hypoglossal nucleus and dorsal motor nucleus of the vagus.
机译:背景氧化应激和大量的一氧化氮(NO)与神经元损伤和神经退行性疾病的病理生理有关。最近的研究表明,(-)-表没食子儿茶素没食子酸酯(EGCG)是一种绿茶多酚,对缺血介导的神经元损伤中自由基介导的脂质过氧化具有有效的抗氧化作用。这项研究的目的是检查EGCG是否会减弱周围神经挤压后下脑干运动神经元中NADPH-d / nNOS的神经元表达。因此,成年幼鼠在挤压其舌下和迷走神经30秒钟(左侧,在颈椎水平)之前,先用EGCG(10、25或50 mg / kg,腹腔内)治疗30分钟。从第1天到第6天继续进行治疗(压碎前剂量的EGCG),并在第3、7、14和28天处死动物。烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPH-d)的组织化学和神经元一氧化氮。合酶(nNOS)免疫组化用于评估迷走神经下舌核和背运动核中神经元NADPH-d / nNOS的表达。

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