Manual Acupuncture Suppresses the Expression of Proinflammatory Proteins Associated with the NLRP3 Inflammasome in the Hippocampus of SAMP8 Mice.

Manual Acupuncture Suppresses the Expression of Proinflammatory Proteins Associated with the NLRP3 Inflammasome in the Hippocampus of SAMP8 Mice.
复制标题

手法针刺抑制 SAMP8 小鼠海马 NLRP3 炎症小体相关促炎蛋白的表达

DOI:
10.1155/2017/3435891
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发表时间:
2017
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Li Z
Li Z
中科院分区:
其他
文献类型:
--
作者:
Ding N;Jiang J;Lu M;Hu J;Xu Y;Liu X;Li Z

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目的探讨手针刺(MA)对NLRP3炎性小体相关蛋白的影响。方法将SAMP8小鼠随机分为阿尔茨海默病(AD)组、MA组和药物组。M组小鼠给予盐酸多奈哌齐0.65 μg/g剂量;MA组在百会(GV20)和印堂(GV29)上应用MA 20 min,然后在水沟(GV26)处针刺。Morris水迷宫法评价大鼠空间学习记忆能力。采用免疫组化染色和western blot方法观察NLRP3炎性小体相关蛋白的表达。结果与正常(N)对照组相比,AD组的空间学习和记忆能力显著降低(p < 0.01)。AD组NLRP3、ASC、Caspase-1、IL-1β阳性染色细胞数量均高于N组,上述蛋白的相对表达量均显著高于N组(p < 0.01)。MA和多奈哌齐均可逆转上述变化(p < 0.01)。结论MA能提高SAMP8小鼠的学习记忆能力。海马NLRP3/Caspase-1通路的负调控可能是MA治疗AD的可能机制。
Objective To investigate the effect of manual acupuncture (MA) on NLRP3 inflammasome-related proteins. Methods SAMP8 mice were randomly divided into Alzheimer's disease (AD) group, the MA group, and the medicine (M) group. Mice in the M group were treated with donepezil hydrochloride at 0.65 μg/g. In the MA group, MA was applied on Baihui (GV20) and Yintang (GV29) for 20 min and then pricked at Shuigou (GV26). The Morris water maze was applied to assess spatial learning and memory. Immunohistochemical staining and western blot analysis were used to observe the expression of NLRP3 inflammasome-related proteins. Results Compared with the normal (N) control group, spatial learning and the memory capabilities of the AD group significantly decreased (p < 0.01). The number of NLRP3, ASC, Caspase-1, and IL-1β positively stained cells in the AD group was higher than the N group, and the relative expression levels of the above proteins were significantly higher than those in the N group (p < 0.01). These changes were reversed by both MA and donepezil (p < 0.01). Conclusion MA can improve the learning and memory capabilities of SAMP8 mice. The negative regulation of the NLRP3/Caspase-1 pathway in the hippocampus may be a possible mechanism of MA in the treatment of AD.
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