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Neuroprotective effects of bee venom acupuncture therapy against rotenone-induced oxidative stress and apoptosis

机译:蜂毒针刺对鱼藤酮诱导的氧化应激和细胞凋亡的神经保护作用

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Parkinson's disease (PD), the most common neurodegenerative movement disorder, is characterized by dopaminergic neurodegeneration, mitochondrial impairment, and oxidative stress. Exposure of animals to rotenone induces a range of responses characteristic of PD, including reactive oxygen species production and dopaminergic cell death. Although L-dopa is the drug of choice for improving core symptoms of PD, it is associated with involuntary movements. The current study was directed to evaluate the neuroprotective effect of bee venom acupuncture therapy (BVA) against rotenone-induced oxidative stress, neuroinflammation, and apoptosis in PD mouse model. Forty male Swiss mice were divided into four groups: (1) received saline solution orally and served as normal control, (2) received rotenone (1.5 mg/kg, s.c. every other day for 6 doses), (3) received rotenone concomitantly with L-dopa (25 mg/kg, daily. p.o. for 6 days), and finally (4) received rotenone concomitantly with BVA (0.02 ml once every 3 days for two weeks). Rotenone-treated mice showed impairment in locomotor behavior and a significant reduction in brain dopamine, serotonin. norepinephrine. GSH levels, and paraoxonase activity, whereas a significant increase was observed in brain malondialdehyde, tumor necrosis factor-alpha, interleukin-beta levels besides DNA damage, and over-expression of caspase-3, Bax, and Bcl-2 genes. Significant improvement of the aforementioned parameters was demonstrated after BVA compared to L-dopa therapy. In conclusion, bee venom normalized all the neuroinflammatory and apoptotic markers and restored brain neurochemistry after rotenone injury. Therefore, BVA is a promising neuroprotective therapy for PD. (C) 2014 Elsevier Ltd. All rights reserved.
机译:帕金森氏病(PD)是最常见的神经退行性运动障碍,其特征是多巴胺能神经变性,线粒体损伤和氧化应激。动物接触鱼藤酮会诱发一系列PD特有的反应特性,包括活性氧的产生和多巴胺能细胞的死亡。尽管左旋多巴是改善PD核心症状的首选药物,但它与不自主运动有关。本研究旨在评估蜂毒针刺疗法(BVA)对鱼藤酮诱导的PD小鼠模型中的氧化应激,神经炎症和细胞凋亡的神经保护作用。 40只瑞士雄性小鼠分为四组:(1)口服生理盐水并作为正常对照组;(2)接受鱼藤酮(1.5 mg / kg,隔日一次,共6剂);(3)伴随接受鱼藤酮L-多巴(25 mg / kg,每天,口服,连续6天),最后(4)与BVA一起接受鱼藤酮(每3天0.02毫升,持续2周)。鱼藤酮治疗的小鼠表现出运动行为受损,脑多巴胺,血清素显着降低。去甲肾上腺素。 GSH水平和对氧磷酶活性,而脑丙二醛,肿瘤坏死因子-α,白细胞介素-β水平除DNA损伤和caspase-3,Bax和Bcl-2基因的过表达外,均显着增加。与左旋多巴疗法相比,BVA后证明了上述参数的显着改善。总而言之,蜂毒在鱼藤酮损伤后能使所有神经炎症和凋亡标记恢复正常,并恢复大脑神经化学。因此,BVA是一种有前途的PD神经保护疗法。 (C)2014 Elsevier Ltd.保留所有权利。

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