Electroacupuncture Pretreatment Alleviates Cerebral Ischemia-Reperfusion Injury by Increasing GSK-3 β Phosphorylation Level via Adenosine A1 Receptor

Wujun Geng; Libin Cai; Kunyuan Han; Ding Li; Yunchang Mo; Qinxue Dai; Hongli Tang; Minyuan Zhang; Percy David Papa Akuetteh; Meita Felicia Balelang; Junlu Wang

doi:10.1155/2020/6848450

Electroacupuncture Pretreatment Alleviates Cerebral Ischemia-Reperfusion Injury by Increasing GSK-3 β Phosphorylation Level via Adenosine A1 Receptor

Biomed Res Int. 2020 Feb 20:2020:6848450. doi: 10.1155/2020/6848450. eCollection 2020.

Authors

Wujun Geng^{1

2}, Libin Cai¹, Kunyuan Han¹, Ding Li¹, Yunchang Mo¹, Qinxue Dai¹, Hongli Tang¹, Minyuan Zhang¹, Percy David Papa Akuetteh¹, Meita Felicia Balelang¹, Junlu Wang^{1

3}

Affiliations

¹ Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
² Department of Anesthesiology, The Yongjia Hospital of TCM, Wenzhou, Zhejiang, China.
³ Department of Anesthesiology, The People's Hospital of Wencheng County, Wenzhou, Zhejiang, China.

Abstract

Objective: To observe the effect of adenosine A1 receptor in the hippocampus of mice on GSK-3β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.

Method: The model of middle cerebral artery occlusion (MCAO) was established and grouped into electroacupuncture pretreatment group (EA group), MCAO group, and sham-operated group (Sham group). The neurobehavioral manifestation, the volume of cerebral infarction, and its related protein changes in mice in each group were observed. Then, adenosine Α1 receptor antagonist and agonist were injected intraperitoneally to observe the effects of A1 receptor on the phosphorylation level of GSK-3β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.

Results: (1) Compared with the MCAO group (24 hours after reperfusion), the infarct size in the EA group decreased significantly, and the Garcia neurological score and phosphorylation level of GSK-3β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury. β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury. β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.

Conclusions: Electroacupuncture pretreatment can increase GSK-3β phosphorylation level via activating A1 receptor, to protect neurons in ischemia-reperfusion injury.β phosphorylation level and elucidate the underlying mechanisms of electroacupuncture pretreatment by activating Α1 receptor mediating cerebral ischemia-reperfusion injury.

MeSH terms

Adenosine A1 Receptor Agonists / pharmacology
Adenosine A1 Receptor Antagonists / pharmacology
Animals
Brain Ischemia / metabolism*
Electroacupuncture*
Glycogen Synthase Kinase 3 beta / metabolism*
Hippocampus / metabolism
Hippocampus / radiation effects
Male
Mice
Mice, Inbred C57BL
Phosphorylation / drug effects
Phosphorylation / radiation effects
Receptor, Adenosine A1 / metabolism*

Substances

Adenosine A1 Receptor Agonists
Adenosine A1 Receptor Antagonists
Receptor, Adenosine A1
Glycogen Synthase Kinase 3 beta
Gsk3b protein, mouse