Electroacupuncture Attenuates Immune-Inflammatory Response in Hippocampus of Rats with Vascular Dementia by Inhibiting TLR4/MyD88 Signaling Pathway.
Electroacupuncture Attenuates Immune-Inflammatory Response in Hippocampus of Rats with Vascular Dementia by Inhibiting TLR4/MyD88 Signaling Pathway.
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DOI：
10.1007/s11655-021-3350-5
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发表时间：
2022-03
影响因子：
2.9
通讯作者：
Tang ZS
中科院分区：
文献类型：
--
作者：
Bu Y;Li WS;Lin J;Wei YW;Sun QY;Zhu SJ;Tang ZS
目的：探讨电针是否通过抑制Toll样受体4(TLR4)/髓系分化因子88(MyD88)信号通路而减轻血管性痴呆(VaD)大鼠海马区免疫炎症反应。实验分3部分进行，按随机数字表法将SD大鼠随机分为假手术组、四血管阻断(4-VO)组、4-VO+电针组、4-VO+非电针组、Sham+电针组、4-VO+脂多糖(LPS)组、4-VO+LPS+EA组、4-VO+TAK-242组。采用4-VO法建立VaD模型。7天后，电针百会、丹中、隔俞、七海、三阴交5穴，每日1次，连续3周。检测淋巴细胞亚群、淋巴细胞转化率和炎性细胞因子白介素6(IL-6)、肿瘤坏死因子α(肿瘤坏死因子α)，以评价VaD大鼠的免疫功能和炎症反应。用透射电子显微镜观察海马神经细胞的超微结构。电针治疗后检测血清TLR4、MYD88、IL-6、肿瘤坏死因子-α水平。侧脑室注射TLR4拮抗剂TAK-242或TLR4激动剂脂多糖后，观察TLR4/MyD88信号转导和认知功能变化。与4-VO组相比，电针能显著改善4-VO+EA组大鼠的免疫功能，抑制大鼠海马区TLR4和MyD88的蛋白和基因表达，降低血清IL-6和肿瘤坏死因子-α的表达(P均<0.05或P<0.01)，并能促进海马神经元的修复。4-VO+LPS+EA组与4-VO+EA组之间、4-VO+TAK-242组与4-VO+EA组之间均无显著差异(P>；0.05)。电针通过抑制TLR4/MyD88信号通路减轻与免疫炎症相关的认知障碍。因此，电针可能是治疗VaD的一种有前途的替代疗法。补充材料(附录1-4)可在本文的在线版本中查阅，网址为10.1007/s1165502133505。
To investigate whether electroacupuncture (EA) alleviates cognitive impairment by suppressing the toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway, which triggers immune-inflammatory responses in the hippocampus of rats with vascular dementia (VaD). The experiments were conducted in 3 parts and in total the Sprague-Dawley rats were randomly divided into 8 groups by a random number table, including sham, four-vessel occlusion (4-VO), 4-VO+EA, 4-VO+non-EA, sham+EA, 4-VO+lipopolysaccharide (LPS), 4-VO+LPS+EA, and 4-VO+TAK-242 groups. The VaD model was established by the 4-VO method. Seven days later, rats were treated with EA at 5 acupoints of Baihui (DV 20), Danzhong (RN 17), Geshu (BL 17), Qihai (RN 6) and Sanyinjiao (SP 6), once per day for 3 consecutive weeks. Lymphocyte subsets, lymphocyte transformation rates, and inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor α(TNF-α) were measured to assess immune function and inflammation in VaD rats. Transmission electron microscopy was used to observe the ultrastructure of nerve cells in the hippocampus. The levels of TLR4, MyD88, IL-6, and TNF-α were detected after EA treatment. TLR4/MyD88 signaling and cognitive function were also assessed after intracerebroventricular injection of TLR4 antagonist TAK-242 or TLR4 agonist LPS with or without EA. Compared with the 4-VO group, EA notably improved immune function of rats in the 4-VO+EA group, inhibited the protein and mRNA expressions of TLR4 and MyD88 in the hippocampus of rats, reduced the expressions of serum IL-6 and TNF-α (all P<0.05 or P<0.01), and led to neuronal repair in the hippocampus. There were no significant differences between the 4-VO+LPS+EA and 4-VO+EA groups, nor between the 4-VO+TAK-242 and 4-VO+EA groups (P>0.05). EA attenuated cognitive impairment associated with immune inflammation by inhibition of the TLR4/MyD88 signaling pathway. Thus, EA may be a promising alternative therapy for the treatment of VaD. Supplementary material (Appendixes 1–4) is available in the online version of this article at 10.1007/s11655-021-3350-5.
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影响因子：
3.6
作者：
Ye, Rensong;Liu, Zhenwei
通讯作者：
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DOI：
10.1038/s41568-019-0153-5
发表时间：
2019-07
期刊：
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