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

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.

Keywords: Aβ; Cognitive deficits; Electroacupuncture; Nitric oxide; Sepsis; eNOS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides* / metabolism
  • Animals
  • Cognitive Dysfunction* / metabolism
  • Cognitive Dysfunction* / therapy
  • Down-Regulation
  • Electroacupuncture*
  • Hippocampus / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nitric Oxide Synthase Type III*
  • Nitric Oxide* / metabolism
  • Sepsis* / metabolism
  • Sepsis* / psychology
  • Sepsis* / therapy
  • Signal Transduction
  • Survivors

Substances

  • Amyloid beta-Peptides
  • Nitric Oxide
  • Nitric Oxide Synthase Type III
  • Nos3 protein, mouse