AccScience Publishing / EJMO / Online First / DOI: 10.36922/EJMO025390416
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ORIGINAL RESEARCH ARTICLE

Protective effects of TianJiangXueshuantongWan on cerebral ischemia–reperfusion injury in rats through the phosphatidylinositol 3-kinase/protein kinase B pathway

XiaoCui Liu1† ,  XiaoXue Miao2† ,  YuChao Bai3 ,  ZiHuan Zhang4 ,  Li Sun5 ,  MingYang Yan6 ,  Hui Han4 ,  WenJie Li5 ,  YuanChen Zhao7 ,  YuXi Xie1*
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1 Department of Intensive Care Medicine, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
2 Department of TCM Master Clinic, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
3 Department of Traditional Chinese Medicine, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
4 Department of Neurology, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
5 Department of Pharmacy, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
6 Emergency Department, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
7 Department of Surgery, Tianjin Beichen Traditional Chinese Medicine Hospital, Tianjin, China
†These authors contributed equally to this work.
EJMO, 025390416 https://doi.org/10.36922/EJMO025390416
Received: 24 September 2025 | Revised: 25 December 2025 | Accepted: 20 January 2026 | Published online: 18 March 2026
© 2026 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution -Noncommercial 4.0 International License (CC-by the license) ( https://creativecommons.org/licenses/by-nc/4.0/ )
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Abstract

Introduction: In China, TianjiangXueshuantongWan (TJXSTW) is widely used clinically to treat cerebral ischemia–reperfusion (I/R) injury. However, the mechanism of its action remains unclear.

Objective: This study investigates whether TJXSTW protects against I/R injury via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.

Methods: A middle cerebral artery occlusion (MCAO)–reperfusion rat model was established. Rats were assigned to a normal (sham) group, MCAO group, MCAO + LY294002 group, MCAO + TJXSTW group, or MCAO + TJXSTW + LY294002 group. Outcomes assessed included brain infarct volume, tissue damage, neuronal apoptosis, mitochondrial structure, and the expression of PI3K/Akt pathway proteins.

Results: TJXSTW mitigated infarct-related tissue damage, neuronal apoptosis, and mitochondrial injury. These protective effects may be attributed to reduced apoptosis via increased expression of phosphorylated Akt and phosphorylated glycogen synthase kinase-3 beta. The use of PI3K pathway inhibitors attenuated the protective effect of TJXSTW on cerebral I/R injury.

Conclusion: TJXSTW exerts a protective effect against cerebral I/R injury by inhibiting apoptosis through the activation of the PI3K/Akt signaling pathway.

Graphical abstract
Keywords
Tianjiang Xueshuantong Wan
Ischemia–reperfusion injury
Phosphatidylinositol 3-kinase pathway
Apoptosis
Funding
None.
Conflict of interest
The authors declare that they have no conflict of interest.
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Eurasian Journal of Medicine and Oncology, Electronic ISSN: 2587-196X Print ISSN: 2587-2400, Published by AccScience Publishing
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