Effects of electroacupuncture on the intestinal thioredoxin interaction protein/Nod-like receptor 3 signaling pathway in mice with Parkinson's disease.

Yao Wang, Yan-Chun Wang, Jun Ma, Ya-Nan Li, Xiao-Lei Zhang, Meng-Ni Hu, Ling Qi, Lei Guo, Zhen Rong, Qing-Ya Guan
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Abstract

Objectives: To observe the effects of electroacupuncture (EA) at "Fengfu" (GV16), "Taichong" (LR3) and "Zusanli" (ST36) on α-synuclein (α-syn), Occludin, Claudin-1, thioredoxin interaction protein (TXNIP) and Nod-like receptor 3 (NLRP3) in Parkinson's disease (PD) mice, so as to investigate the mechanisms of EA on intestinal barrier function and inflammation in PD mice.

Methods: Thirty six C57BL/6 mice were randomly divided into control, model and EA groups, with 12 mice in each group. PD mice model was induced by rotenone intragastric administration for 28 days. Mice in the EA group were treated with EA (2 Hz, 1 mA) at GV16, LR3 and ST36 for 30 min, once a day for 14 days. The behavioral scores were observed. The total distance of autonomic movement was measured by open field test. The expression level of α-syn in substantia nigra and colon tissue was determined by immunohistochemistry. The colonic morphology and goblet cell distribution were observed by Alcian blue staining. The expression levels of Occludin, Claudin-1, TXNIP and NLRP3 mRNA in colon tissue were detected by real-time fluorescence quantitative PCR.

Results: Compared with the control group, the behavioral scores of rats were increased (P<0.01);the total distance of autonomous movement was decreased (P<0.01);the positive expression level of α-syn in the substantia nigra and colon was increased (P<0.01);the goblet cells and crypts in colon tissue were reduced, and the muscular layer was thinner;the expression levels of Occludin and Claudin-1 mRNAs in colon tissue were decreased (P<0.01) while TXNIP and NLRP3 mRNAs were increased (P<0.01) in the model group. Compared with the model group, the surface villi of colon tissue was more complete, the goblet cells and crypts were increased, and the muscular layer was thickened;the other indexes were reversed (P<0.01, P<0.05) in the EA group.

Conclusions: EA at GV16, LR3 and ST36 can reduce the abnormal accumulation of α-syn in the substania nigra and colon tissue of PD mice, alleviate the damage of intestinal barrier, regulate TXNIP/NLRP3 signaling pathway, so as to delay the occurrence and development of PD.

电针对帕金森病小鼠肠道硫氧还蛋白相互作用蛋白/Nod样受体3信号通路的影响。
目的:观察电针“风府”、“太冲”、“足三里”对帕金森病(PD)小鼠α-突触核蛋白(α-syn)、Occludin、Claudin-1、硫氧还蛋白相互作用蛋白(TXNIP)和Nod样受体3(NLRP3)的影响,探讨电针对PD小鼠肠道屏障功能和炎症反应的影响机制。方法:36只C57BL/6小鼠随机分为对照组、模型组和电针组,每组12只。鱼藤酮灌胃诱导PD小鼠模型28天。电针组小鼠用GV16、LR3和ST36的电针(2Hz,1mA)治疗30分钟,每天一次,持续14天。观察行为评分。自主运动的总距离采用开放性场地试验测定。免疫组织化学方法检测黑质和结肠组织中α-syn的表达水平。阿尔西安蓝染色观察结肠形态及杯状细胞分布。采用实时荧光定量PCR检测Occludin、Claudin-1、TXNIP和NLRP3mRNA在结肠组织中的表达水平,结论:电针GV16、LR3和ST36可减少帕金森病小鼠黑质及结肠组织中α-syn的异常积聚,减轻肠屏障损伤,调节TXNIP/NLRP3信号通路,延缓帕金森病的发生和发展。
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