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The neuroprotective mechanism of 2-arachidonoylglycerol 2-AG against non-caspase-dependent apoptosis in mice hippocampal neurons following MCAO

Authors Zhong HY, Yang Z, Qiu Z, Lei SQ, Xia ZY

Received 9 March 2019

Accepted for publication 23 July 2019

Published 23 August 2019 Volume 2019:15 Pages 2417—2424

DOI https://doi.org/10.2147/NDT.S208094

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yuping Ning


He-Ying Zhong, Zhou Yang, Zhen Qiu, Shao-Qing Lei, Zhong-Yuan Xia

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, People’s Republic of China

Correspondence: Zhong-Yuan Xia
Department of Anesthesiology, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuhan 430060, Hubei Province, People’s Republic of China
Tel +86 1 380 862 8560
Email xiazhongyuan2005@aliyun.com

Objective: In this study, the neuroprotective mechanism of 2-arachidonoylglycerol 2-AG against non-caspase-dependent apoptosis in mice hippocampal neurons following MCAO was investigated.
Method: One hundred and fifty healthy clean male C57BL/6 mice were randomly divided into 3 groups: sham group, model group and 2-AG treatment group, 50 mice in each group. A modified Zea Longa method was used to establish a model of middle cerebral artery occlusion (MCAO) in mice. The apoptosis rate and mitochondrial membrane potential of hippocampal nerve cells were measured by flow cytometry. The mRNA expressions of AIF, Endo G and BNIP3 in hippocampal tissues were determined by qPCR. Western blot was used to determine the protein expressions of AIF, Endo G and BNIP3 in the mitochondria of hippocampal tissue.
Results: The apoptosis rate of hippocampal neurons in the group treated with 2-AG was significantly lower than that of the model (P<0.01), which indicated that 2-AG could inhibit the apoptosis of hippocampal neurons induced by MCAO. However, the mitochondrial membrane potential of hippocampal neurons in the group treated with 2-AG was significantly higher than that of the model (P<0.01), indicating that 2-AG could improve the mitochondrial membrane potential of hippocampal neurons in MCAO mice. Real-time quantitative PCR (qPCR) showed that 2-AG could inhibit the gene expressions of AIF, Endo G and BNIP3 in hippocampal tissues. Western blot results showed that 2-AG could inhibit the secretions of AIF, Endo G and BNIP3 into cytoplasm in mitochondria.
Conclusion: Endocannabinoids 2-AG had a protective effect on neurons injury, and the mechanism was possibly associated with the protection of the brain nerve cells in the hippocampus and the integrity of the mitochondrial function. Endocannabinoids 2-AG may inhibit the non-caspase-dependent apoptosis pathway, so as to exert its nerve protective effect.

Keywords: 2-arachidonoylglycerol, hippocampus, nerve cell, non-caspase-dependent pathway

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