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烟碱样胆碱能通路对胶原性关节炎大鼠的作用研究

Study on effects of nicotin cholinergic pathway on collagen induced arthritis in rats
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摘要 目的探讨烟碱样胆碱能通路对胶原性关节炎(CIA)的作用,为关节炎等自身免疫性疾病寻找新的治疗途径。方法建立大鼠CIA模型,将模型大鼠分为迷走神经刺激(VNS)组和假手术组,VNS组在完全清醒状态下给予持续迷走神经刺激(5v,2ms,1HZ),每天30min,共4周。观察2组大鼠的病理和关节炎指数变化,用免疫组织化学和RT-PCR技术检测大鼠烟碱样乙酰胆碱受体α7亚单位(nAChRα7)和胆碱乙酰转移酶(ChAT)及乙酰胆碱酯酶(AChE)在关节滑膜的蛋白和基因表达。结果治疗4周后,VNS组大鼠关节炎指数明显低于假手术组(P<0.01);VNS组大鼠踝关节组织病理改善明显高于假手术组(P<0.01);免疫组化和RT-PCR检测nAChRα7、ChAT蛋白和mRNA表达均明显高于假手术组(P<0.01);各组大鼠AChE蛋白和基因水平表达均差异无显著性(P>0.05)。结论电刺激迷走神经可以上调nAChRα7、ChAT基因在免疫组织的表达,减轻胶原性关节炎大鼠的炎症,提示烟碱样胆碱能通路在治疗胶原性关节炎中有重要作用。 [Objective] To explore effects of nicotin cholinergic pathway on collagen induced arthritis in rats. [Methods] Rats model of collagen induced arthritis (CIA) was duplicated by intradermal injection of type Ⅱ collagen, the rats were devided into three groups: vagus nerve stimulation (VNS) group, sham operation group and normal control group. Rats in group VNS were stimulated at the left cervical vagus nerves for 30 minutes a day with constant square wave, pulse current with intratrain of 16 Hz, pulse duration of 1.0 ms, train duration of 10 s, interstimulus interval of 1.Stain and intensities of 3.0mA. Then immunohistoehemieal and RT-PCR methods were used to detect the nicotinic aeetyleholine receptors α7(nAChRα7), choline aeetyltransferase (CHAT) and aeetyleholinesterase (ACHE) in Synovium. [Results] In group VNS, the expression of nAChRα7 and ChAT was significantly higher than that in Sham operated (P 〈0.01); there was no apparent difference in the expression of AChE of the three groups (P 〉0.05). [Conclusion] Vagus nerve stimulation can up-regulate the expression of nAChRα7and ChAT in the immune tissues, activate the eholinergie system in immune system, and reduce the inflammation of the rats with CIA.
出处 《中国现代医学杂志》 CAS CSCD 北大核心 2008年第3期328-331,334,共5页 China Journal of Modern Medicine
关键词 迷走神经 电刺激 烟碱样乙酰胆碱受体α7亚单位 胶原性关节炎 vagus nerve stimulation electro-stimulation nicotinic aeetyleholine receptors alpha7(nAChRα7) choline aeetyltransferase (CHAT) collagen induced arthritis
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