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首页> 外文期刊>Experimental Neurology >Acupuncture prevents 6-hydroxydopamine-induced neuronal death in the nigrostriatal dopaminergic system in the rat Parkinson's disease model.
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Acupuncture prevents 6-hydroxydopamine-induced neuronal death in the nigrostriatal dopaminergic system in the rat Parkinson's disease model.

机译:在帕金森病大鼠模型中,针灸可防止6-羟基多巴胺诱导的黑质纹状体多巴胺能系统神经元死亡。

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摘要

Parkinson's disease (PD) is a chronic neurodegenerative disorder, and it has been suggested that treatments promoting survival and functional recovery of affected dopaminergic neurons could have a significant and long-term therapeutic value. In the present study, we investigated the neuroprotective effects of acupuncture on the nigrostriatal system in rat unilaterally lesioned with 6-hydroxydopamine (6-OHDA, 4 microg/microl, intrastriatal injection) using tyrosine hydroxylase (TH) and receptor for brain-derived neurotrophic factor, trkB, immunohistochemistries. Two weeks after the lesions were made, rats presented with asymmetry in rotational behavior (118.3 +/- 17.5 turns/h) following injection with apomorphine, a dopamine receptor agonist (0.5 mg/kg, sc). In contrast, acupunctural treatment at acupoints GB34 and LI3 was shown to significantly reduce this motor deficit (14.6 +/- 13.4 turns/h). Analysis via TH immunohistochemistry revealed a substantial loss of cell bodies in the substantia nigra (SN) (45.7% loss) and their terminals in the dorsolateral striatum ipsilateral to the 6-OHDA-induced lesion. However, acupunctural treatment resulted in the enhanced survival of dopaminergic neurons in the SN (21.4% loss) and their terminals in the dorsolateral striatum. Acupuncture also increased the expression of trkB significantly (35.6% increase) in the ipsilateral SN. In conclusion, we observed that only acupuncturing without the use of any drug has the neuroprotective effects against neuronal death in the rat PD model and these protective properties of acupuncture could be mediated by trkB.
机译:帕金森氏病(PD)是一种慢性神经退行性疾病,已提出促进受累多巴胺能神经元存活和功能恢复的治疗方法可能具有重要的长期治疗价值。在本研究中,我们研究了酪氨酸羟化酶(TH)和受体对脑源性神经营养的针刺对6-羟基多巴胺(6-OHDA,4微克/微升,纹状体内注射)单侧病变的大鼠黑质纹状体系统的神经保护作用。因子,trkB,免疫组织化学。损伤形成后两周,大鼠注射多巴胺受体多巴胺吗啡(0.5 mg / kg,皮下注射)后,在旋转行为方面表现出不对称性(118.3 +/- 17.5转/小时)。相比之下,针灸治疗GB34和LI3穴位可显着减少运动障碍(14.6 +/- 13.4转/小时)。通过TH免疫组织化学的分析表明,黑质(SN)中的细胞体大量丢失(损失了45.7%),而在6-OHDA诱导的病变的同侧的背外侧纹状体中则出现了末端。然而,针灸治疗导致SN中多巴胺能神经元及其背侧纹状体末端的存活增加(损失21.4%)。针灸还显着增加了同侧SN中trkB的表达(增加了35.6%)。总之,我们观察到在不使用任何药物的情况下,针刺对大鼠PD模型的神经元死亡具有神经保护作用,而tkB可以介导针刺的这些保护特性。

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