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Protective effects of Berberine on hippocampal neurons after ischemia in vivo and in vitro
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DOI：10.1186/s12906-026-05479-z.png)
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Abstract
En 中文
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. 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. 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. 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.
Keywords:
Ischemia
Berberine
Oxygen glucose deprivation
Apoptosis
Phospho-Akt
Journal
B
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3.4
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273
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Cited Papers