Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice.
Electroacupuncture ameliorates postoperative cognitive dysfunction and associated neuroinflammation via NLRP3 signal inhibition in aged mice.
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电针通过抑制 NLRP3 信号改善老年小鼠术后认知功能障碍和相关神经炎症。
DOI：
10.1111/cns.13784
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发表时间：
2022-03
影响因子：
5.5
通讯作者：
Song J
中科院分区：
文献类型：
--
作者：
Sun L;Yong Y;Wei P;Wang Y;Li H;Zhou Y;Ruan W;Li X;Song J
术后认知功能障碍（POCD）与预后恶化相关，尤其是在老年人群中。临床和动物实验表明，电针可以改善POCD。然而，其机制，尤其是EA对炎性小体的调节作用尚不清楚。通过对18月龄小鼠进行部分肝切除术，术后电针或不电针百会穴（GV 20）7天，建立POCD模型。通过Morris水迷宫试验评估认知功能，并通过qPCR、ELISA或免疫组织化学测定促炎细胞因子IL-1β和IL-6以及小胶质细胞活性。通过蛋白质印迹法评价紧密连接蛋白、NLRP 3炎性体和下游蛋白以及NF-κB途径蛋白。EA显著地保留了POCD小鼠的认知功能障碍，与神经炎症的抑制相关，如通过减少小胶质细胞活化和降低脑组织中的IL-1β和IL-6水平所证明的。EA还保存了海马神经元和紧密连接蛋白ZO-1和claudin 5。电针抑制NLRP 3炎性小体和NF-κB的活化，而NLRP 3活化则消除了电针对认知功能的治疗作用。电针治疗POCD介导的认知功能障碍与改善神经炎症相关。从机制上讲，EA的治疗效果依赖于NLRP 3抑制。EA可缓解PND介导的认知功能障碍，并改善神经炎症。从机制上讲，EA的治疗效果依赖于NLRP 3激活。
Postoperative cognitive dysfunction (POCD) is associated with worsened prognosis especially in aged population. Clinical and animal studies suggested that electroacupuncture (EA) could improve POCD. However, the underlying mechanisms especially EA’s regulatory role of inflammasomes remain unclear. The model of POCD was established by partial hepatectomy surgery in 18‐month mice with or without postoperative EA treatment to the Baihui acupoint (GV20) for 7 days. Cognitive functions were assessed by Morris water maze test, and proinflammatory cytokines IL‐1β and IL‐6 and microglia activity were assayed by qPCR, ELISA, or immunohistochemistry. Tight junction proteins, NLRP3 inflammasome and downstream proteins, and NF‐κB pathway proteins were evaluated by western blotting. EA markedly preserved cognitive dysfunctions in POCD mice, associated with the inhibition of neuroinflammation as evidenced by reduced microglial activation and decreased IL‐1β and IL‐6 levels in brain tissue. EA also preserved hippocampal neurons and tight junction proteins ZO‐1 and claudin 5. Mechanistically, the activation of NLRP3 inflammasome and NF‐κB was inhibited by EA, while NLRP3 activation abolished EA’s treatment effects on cognitive function. EA alleviates POCD‐mediated cognitive dysfunction associated with ameliorated neuroinflammation. Mechanistically, EA’s treatment effects are dependent on NLRP3 inhibition. EA alleviates PND‐mediated cognitive dysfunction associated with ameliorated neuroinflammation. Mechanistically, EA’s treatment effects are dependent on NLRP3 activation.
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影响因子：
2.3
作者：
Evered LA;Goldstein PA
通讯作者：
Goldstein PA
电针可能通过下调 Notch 信号通路抑制 AD 模型大鼠的神经元凋亡并改善认知障碍
DOI：
10.1155/2015/393569
发表时间：
2015
期刊：
Evidence-based complementary and alternative medicine : eCAM
影响因子：
--
作者：
Guo HD;Tian JX;Zhu J;Li L;Sun K;Shao SJ;Cui GH
通讯作者：
Cui GH
影响因子：
6.3
作者：
Chi, Laiting;Du, Kairong;Li, Wenzhi
通讯作者：
Li, Wenzhi
影响因子：
15.9
作者：
Guo, De-Huang;Yamamoto, Masaki;Stranahan, Alexis M.
通讯作者：
Stranahan, Alexis M.
影响因子：
1.9
作者：
Greene, AK;Puder, M
通讯作者：
Puder, M