Protective effects of Berberine on hippocampal neurons after ischemia in vivo and in vitro.
6 affiliations
- 1Department of Neurology, The Affiliated Shunde Hospital of Jinan University, Foshan, Guangdong, China.
- 2Department of Cerebrovascular Disease Center, Zhuhai Hospital Affiliated With Jinan University (Zhuhai People's Hospital), Zhuhai, 519000, Guangdong, China.
- 3Department of Neurology and Stroke Center, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China.
- 4Department of Pharmacy, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China. [email protected].
- 5Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, Guangdong, China. [email protected].
- 6Department of Neurology and Stroke Center, The First Affiliated Hospital of Jinan University, Guangzhou, 510632, Guangdong, China. [email protected].
Abstract
Background
Apoptosis plays a pivotal role in neuronal death following ischemic brain injury. Berberine (BBR), a natural isoquinoline alkaloid extracted from Coptis chinensis, exhibits multiple biological activities and has shown neuroprotective effects in experimental ischemia models. However, its direct protective effects on neurons and the underlying apoptosis-related mechanisms remain to be fully clarified.Methods
A transient forebrain ischemia model was established in mice to evaluate the neuroprotective effects of BBR in vivo. Cognitive function was assessed using the Y-maze test, and hippocampal neuronal injury was examined by H&E staining. In vitro, primary hippocampal neurons were subjected to oxygen-glucose deprivation (OGD) to mimic ischemic injury. Neuronal viability, mitochondrial function, intracellular calcium levels, apoptosis, and related signaling pathways were analyzed using CCK-8, LDH, JC-1, Fluo-4 AM, Hoechst staining, caspase-3 activity assay, and Western blotting.Results
BBR significantly reduced hippocampal neuronal loss and improved cognitive deficits in mice after transient forebrain ischemia. In primary hippocampal neurons exposed to OGD, BBR markedly enhanced cell viability, alleviated mitochondrial dysfunction, attenuated intracellular calcium overload, and suppressed neuronal apoptosis. Mechanistically, BBR may increase the expression of phospho-Akt and Bcl2 while reducing the expression of Bax and the activity of cleaved caspase-3.Conclusions
These findings demonstrate that berberine exerts significant neuroprotective effects against ischemia-induced neuronal injury by targeting apoptosis-related signaling pathways, particularly the Akt/caspase-3 axis, and support its potential as a therapeutic candidate for ischemic stroke.
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BibTeX
@article{li2026protective,
title = {{Protective effects of Berberine on hippocampal neurons after ischemia in vivo and in vitro.}},
author = {Xiaoying Li and Zhangpei Liu and Longyan Lu and Qizhi Zhong and Yuying Wu and Ying Yang and Zheng Zhang and Zhongshan Shi and Dawei Dong},
journal = {BMC complementary medicine and therapies},
year = {2026},
month = jul,
doi = {10.1186/s12906-026-05479-z},
url = {https://europepmc.org/article/MED/42928173},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Protective effects of Berberine on hippocampal neurons after ischemia in vivo and in vitro.
AU - Xiaoying Li
AU - Zhangpei Liu
AU - Longyan Lu
AU - Qizhi Zhong
AU - Yuying Wu
AU - Ying Yang
AU - Zheng Zhang
AU - Zhongshan Shi
AU - Dawei Dong
PY - 2026
DA - 2026/07/28
JO - BMC complementary medicine and therapies
DO - 10.1186/s12906-026-05479-z
UR - https://europepmc.org/article/MED/42928173
AB - Background Apoptosis plays a pivotal role in neuronal death following ischemic brain injury. Berberine (BBR), a natural isoquinoline alkaloid extracted from Coptis chinensis, exhibits multiple biological activities and has shown neuroprotective effects in experimental ischemia models. However, its direct protective effects on neurons and the underlying apoptosis-related mechanisms remain to be fully clarified.Methods A transient forebrain ischemia model was established in mice to evaluate the neuroprotective effects of BBR in vivo. Cognitive function was assessed using the Y-maze test, and hippocampal neuronal injury was examined by H&E staining. In vitro, primary hippocampal neurons were subjected to oxygen-glucose deprivation (OGD) to mimic ischemic injury. Neuronal viability, mitochondrial function, intracellular calcium levels, apoptosis, and related signaling pathways were analyzed using CCK-8, LDH, JC-1, Fluo-4 AM, Hoechst staining, caspase-3 activity assay, and Western blotting.Results BBR significantly reduced hippocampal neuronal loss and improved cognitive deficits in mice after transient forebrain ischemia. In primary hippocampal neurons exposed to OGD, BBR markedly enhanced cell viability, alleviated mitochondrial dysfunction, attenuated intracellular calcium overload, and suppressed neuronal apoptosis. Mechanistically, BBR may increase the expression of phospho-Akt and Bcl2 while reducing the expression of Bax and the activity of cleaved caspase-3.Conclusions These findings demonstrate that berberine exerts significant neuroprotective effects against ischemia-induced neuronal injury by targeting apoptosis-related signaling pathways, particularly the Akt/caspase-3 axis, and support its potential as a therapeutic candidate for ischemic stroke.
SN - 2662-7671
ER -