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电针治疗通过激活 eNOS/NO 通路和相关的 Aβ下调改善脓毒症幸存者小鼠的长期认知障碍。

Electroacupuncture treatment ameliorated the long-term cognitive impairment via activating eNOS/NO pathway and related Aβ downregulation in sepsis-survivor mice.

机构信息

Department of Anesthesiology, Shuguang Hospital Affiliated with Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China.

Research Institute of Acupuncture Anesthesia, Shuguang Hospital Affiliated with Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China.

出版信息

Physiol Behav. 2022 Jan 1;243:113646. doi: 10.1016/j.physbeh.2021.113646. Epub 2021 Nov 12.

Abstract

OBJECTIVE

Sepsis is a major challenge in intensive care unit worldwide and the septic survivors are left with long-term cognitive deficits. This work aims to explore the effects of electroacupuncture (EA) on long-term cognitive function and its underlying mechanism in sepsis-survivor mice.

METHODS

Sepsis was induced by cecal ligation and puncture in C57BL/6 male mice. Seven days post-surgery, sepsis-survivor mice were treated with EA or nonacupoint EA for 17 days twice daily. Then, cognitive function was evaluated by Morris water maze task. The hippocampus tissue were collected from the mice at 30 days post-surgery. The level of nitric oxide and the expression of endothelial nitric oxide (eNOS), phospho-eNOS (p-eNOS), and amyloid β-peptide (Aβ) were measured.

RESULTS

Compared with the sham-operated control, sepsis-survivors had significant cognitive deficits evidenced by the increased time of escape latency and reduced crossing number in Morris water maze task, as well as lower NO and p-eNOS level and higher Aβ level. EA treatment at GV20 and ST36 acupoints but not at a nonacupoint improved the cognitive function, increased the NO and p-eNOS level, and decreased Aβ generation; while eNOS inhibitor (l-NAME) undermined the efficacy of EA treatment.

CONCLUSION

In conclusion, repeated EA treatment could ameliorate the long-term cognitive impairment via manipulating the expression of p-eNOS and related Aβ in sepsis-survivor mice.

摘要

目的

脓毒症是全球重症监护病房的重大挑战,脓毒症幸存者会留下长期认知缺陷。本研究旨在探讨电针对脓毒症幸存者小鼠长期认知功能的影响及其潜在机制。

方法

采用盲肠结扎穿孔法诱导雄性 C57BL/6 小鼠脓毒症。术后 7 天,脓毒症幸存者小鼠接受电针(EA)或非穴位 EA 治疗,每天 2 次,共 17 天。然后通过 Morris 水迷宫任务评估认知功能。术后 30 天,从小鼠中采集海马组织。测量一氧化氮(NO)水平以及内皮型一氧化氮合酶(eNOS)、磷酸化内皮型一氧化氮合酶(p-eNOS)和淀粉样β肽(Aβ)的表达。

结果

与假手术对照组相比,脓毒症幸存者在 Morris 水迷宫任务中的逃避潜伏期时间延长、穿越平台次数减少,表明存在明显的认知功能障碍,同时 NO 和 p-eNOS 水平降低,Aβ 水平升高。GV20 和 ST36 穴位的 EA 治疗(而非非穴位)改善了认知功能,增加了 NO 和 p-eNOS 水平,并减少了 Aβ 的生成;而 eNOS 抑制剂(l-NAME)削弱了 EA 治疗的效果。

结论

综上所述,重复 EA 治疗可通过调节脓毒症幸存者小鼠 p-eNOS 的表达和相关 Aβ,改善长期认知障碍。

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