Basic Study
Copyright ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Psychiatry. Sep 19, 2023; 13(9): 620-629
Published online Sep 19, 2023. doi: 10.5498/wjp.v13.i9.620
Hippocampus protection from apoptosis by Baicalin in a LiCl-pilocarpine-induced rat status epilepticus model through autophagy activation
Bin Yang, Han-Yu Wen, Ri-Sheng Liang, Ting-Ming Lu, Zheng-Yan Zhu, Chun-Hua Wang
Bin Yang, Han-Yu Wen, Ting-Ming Lu, Zheng-Yan Zhu, Chun-Hua Wang, Department of Neurosurgery, Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian Province, China
Ri-Sheng Liang, Department of Neurosurgery, Affiliated Union Hospital of Fujian Medical University, Neurosurgery Research Institute of Fujian Province, Fuzhou 350001, Fujian Province, China
Author contributions: Yang B and Wen HY contributed equally to this work; Yang B and Wen HY proposed the overall research goal and designed the research plan and model design; Yang B, Wen HY, Liang RS, and Lu TM conducted feasibility analysis, review, and supervision of the experiment; Yang B, Wen HY, Zhu ZY, and Wang CH conducted statistical processing and analysis of the data; Yang B and Wen HY are responsible for writing the first draft of the paper; Yang B, Wen HY, and Liang RS were responsible for the review, revision, and quality control of the paper; all authors determined the final draft of the paper.
Supported by Natural Science Foundation of Fujian Province of China, No. 2019J01317.
Institutional animal care and use committee statement: The Institutional Animal Care, Ethics, and Use Committees of Fujian Medical University (Fuzhou, China) approved all animal experiments, No. 2018-062.
Conflict-of-interest statement: The authors declare no competing interests.
Data sharing statement: The datasets generated and analyzed during the current study are available from the corresponding author upon reasonable request.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ri-Sheng Liang, PhD, Professor, Department of Neurosurgery, Affiliated Union Hospital of Fujian Medical University, Neurosurgery Research Institute of Fujian Province, No. 29 Xinquan Road, Fuzhou 350001, Fujian Province, China. doctorlr@126.com
Received: May 19, 2023
Peer-review started: May 19, 2023
First decision: June 1, 2023
Revised: July 4, 2023
Accepted: July 28, 2023
Article in press: July 28, 2023
Published online: September 19, 2023
Processing time: 119 Days and 0.7 Hours
Abstract
BACKGROUND

Autophagy is associated with hippocampal injury following status epilepticus (SE) and is considered a potential therapeutic mechanism. Baicalin, an emerging multitherapeutic drug, has shown neuroprotective effects in patients with nervous system diseases due to its antioxidant properties.

AIM

To investigate the potential role of autophagy in LiCl-pilocarpine-induced SE.

METHODS

The drugs were administered 30 min before SE. Nissl staining showed that Baicalin attenuated hippocampal injury and reduced neuronal death in the hippocampus. Western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling assay confirmed that Baicalin reversed the expression intensity of cleaved caspase-3 and apoptosis in hippocampal CA1 following SE. Fur-thermore, western blotting and immunofluorescence staining were used to measure the expression of autophagy markers (p62/SQSTM1, Beclin 1, and LC3) and apoptotic pathway markers (cleaved caspase-3 and Bcl-2).

RESULTS

Baicalin significantly upregulated autophagic activity and downregulated mitochondrial apoptotic pathway markers. Conversely, 3-methyladenine, a commonly used autophagy inhibitor, was simultaneously administered to inhibit the Baicalin-induced autophagy, abrogating the protective effect of Baicalin on the mitochondrial apoptotic level.

CONCLUSION

We illustrated that Baicalin-induced activation of autophagy alleviates apoptotic death and protects the hippocampus of SE rats.

Keywords: Baicalin; Status epilepticus; Autophagy; Mitochondrial apoptosis

Core Tip: This study established the rat model of status epilepticus by intraperitoneally injecting LiCl-pilocarpine. Then, Baicalin was administered to the rats for treatment. The pathological changes of hippocampal were observed. Western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling assays were used to verify the inhibitory effect of Baicalin on apoptosis of rat hippocampal neuronal cells. We have drawn the conclusion that Baicalin protects the hippocampus from apoptosis.