Electroacupuncture Relieves Hippocampal Injury by Heme Oxygenase-1 to Improve Mitochondrial Function

Rui Mu; Na Li; Jian-Bo Yu; Li-Rong Gong; Shu-An Dong; Jia Shi; Yuan Zhang; Zi-Lei Xie

doi:10.1016/j.jss.2021.12.013

Electroacupuncture Relieves Hippocampal Injury by Heme Oxygenase-1 to Improve Mitochondrial Function

J Surg Res. 2022 May:273:15-23. doi: 10.1016/j.jss.2021.12.013. Epub 2022 Jan 10.

Authors

Rui Mu¹, Na Li², Jian-Bo Yu³, Li-Rong Gong², Shu-An Dong², Jia Shi², Yuan Zhang², Zi-Lei Xie²

Affiliations

¹ Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, P.R. China; Department of Anesthesiology and Critical Care Medicine, Nankai University Affiliated Nankai Hospital, Tianjin, P.R. China.
² Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, P.R. China.
³ Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, P.R. China. Electronic address: 30717008@nankai.edu.cn.

PMID: 35016152
DOI: 10.1016/j.jss.2021.12.013

Abstract

Introduction: Electroacupuncture (EA) treatment has been demonstrated to have the potential to prevent sepsis-induced hippocampal injury; however, the mechanisms underlying the protective effects of EA against such injury remain unclear. Herein, to elucidate these mechanisms, we constructed a mouse model of lipopolysaccharide (LPS)-induced hippocampal injury to investigate the protection mechanism of EA and to determine whether heme oxygenase-1 (HO-1)-mediated mitochondrial function is involved in the protective effect of EA.

Materials and methods: The sepsis model of hippocampal injury was induced by administering LPS. The Zusanli and Baihui acupoints were stimulated using EA for 30 min once a day, for 5 d before LPS exposure and the first day after administering LPS. Hippocampal injury was investigated by hematoxylin and eosin staining and Nissl staining. HO-1 levels were measured using Western blotting. Mitochondrial metabolism was validated by assessing adenosine triphosphate, superoxide dismutase, malondialdehyde levels, reactive oxygen species production, and mitochondrial respiratory chain activity. Mitochondrial morphology was analyzed by transmission electron microscopy.

Results: EA treatment alleviated neuronal injury, impeded oxidative stress, and improved mitochondrial respiratory function, energy metabolism, and mitochondrial morphology in LPS-exposed mice. In addition, HO-1 knockout aggravated LPS-induced hippocampal injury, aggravated oxidative stress, and reduced mitochondrial respiratory function and aggravated mitochondrial swelling, crest relaxation, and vacuole degeneration. Moreover, EA was unable to reverse the hippocampal damage and mitochondrial dysfunction caused by LPS exposure after HO-1 knockout.

Conclusions: EA improves LPS-induced hippocampal injury by regulating HO-1-mediated mitochondrial function. Furthermore, HO-1 plays a critical role in maintaining mitochondrial function and resisting oxidative injury.

Keywords: Electroacupuncture; Heme oxygenase-1; Hippocampal injury; Lipopolysaccharide; Mitochondrial function.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Electroacupuncture*
Heme Oxygenase-1 / metabolism
Hippocampus / metabolism
Lipopolysaccharides
Mice
Mitochondria / metabolism
Oxidative Stress
Sepsis* / metabolism
Sepsis* / therapy

Substances

Lipopolysaccharides
Heme Oxygenase-1