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Repetitive transcranial magnetic stimulation for treatment of lactacystin-induced Parkinsonian rat model

机译:重复经颅磁刺激治疗乳腺素诱发的帕金森病大鼠模型

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摘要

The dysfunction of ubiquitin-proteasome system is an important pathogenesis in the neurodegenerative process of Parkinson's disease. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and potential method in treating Parkinson's disease. To investigate whether rTMS has neuroprotective effects in parkinsonian rat model induced by ubiquitin-proteasome system impairment, we gave rTMS daily for 4 weeks to proteasome inhibitor, lactacystin-induced parkinsonian rat model. Rotational behavior test demonstrated that rTMS obviously reduced apomorphine-induced turning number in parkinsonian rats. rTMS could significantly alleviate the loss of tyrosine hydroxylase-positive dopaminergic neurons in lactacystin-lesioned substantia nigra and prevent the loss of striatal dopamine levels. Furthermore, rTMS also reduced the levels of apoptotic protein (cleaved caspase-3) and inflammatory factors (cyclooxygenase-2 and tumor necrosis factor alpha) in lesioned substantia nigra. These results suggest that rTMS can protect nigral dopaminergic neurons against the ubiquitin-proteasome system impairment-induced degeneration by anti-apoptotic and anti-inflammatory molecular mechanism.
机译:泛素-蛋白酶体系统功能异常是帕金森氏病神经退行性病变的重要发病机制。重复经颅磁刺激(rTMS)是治疗帕金森氏病的一种非侵入性且潜在的方法。为了研究rTMS是否在泛素-蛋白酶体系统损伤所致的帕金森病大鼠模型中具有神经保护作用,我们将蛋白酶体抑制剂,乳腺素诱发的帕金森病大鼠模型每天给予rTMS 4周。旋转行为测试表明,rTMS明显降低了阿朴吗啡诱导的帕金森病大鼠转数。 rTMS可以显着减轻乳突质病变黑质中酪氨酸羟化酶阳性多巴胺能神经元的丢失,并防止纹状体多巴胺水平的丢失。此外,rTMS还降低了病变黑质中凋亡蛋白(裂解的caspase-3)和炎性因子(环氧合酶2和肿瘤坏死因子α)的水平。这些结果表明,rTMS可以通过抗凋亡和抗炎分子机制保护黑质多巴胺能神经元免受泛素-蛋白酶体系统损伤诱导的变性。

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