Related Experiment Video
Updated: Jun 17, 2026
Exploring the Two Herb Combination Strategy to Treat Injured PC12 Cells
Published on: November 18, 2022
Neuroprotection by baicalein in ischemic brain injury involves PTEN/AKT pathway
1Department of Pharmacology, Pharmaceutical College, Xianning University, Xianning, China.
Abstract:
Recently more evidences support baicalein (Bai) is neuroprotective in models of ischemic stroke. This study was conducted to determine the molecular mechanisms involved in this effect. Either permanent or transient (2 h) middle cerebral artery occlusion (MCAO) was induced in rats in this study. Permanent MCAO led to larger infarct volumes in contrast to transient MCAO. Only in transient MCAO, Bai administration significantly reduced infarct size. Baicalein also markedly reduced apoptosis in the penumbra of transient MCAO rats. Additionally, oxygen and glucose deprivation (OGD) was used to mimic ischemic insult in primary cultured cortical neurons. A rapid increase in the intracellular reactive oxygen species level and nitrotyrosine formation induced by OGD was counteracted by Bai, which is parallel with attenuated cell injury. The reduction of phosphorylation Akt and glycogen synthase kinase-3beta (GSK3beta) induced by OGD was restored by Bai, which was associated with preserved levels of phosphorylation of PTEN, the phophatase that negatively regulates Akt. As a consequence, Bcl-2/Bcl-xL-associated death protein phosphorylation was increased and the protein level of Bcl-2 in motochondria was maintained, which subsequently antagonize cytochrome c released in cytosol. LY294002 blocked the increase in phospho-AKT evoked by Bai and abolished the associated protective effect. Together, these findings provide evidence that Bai protects neurons against ischemia injury and this neuroprotective effect involves PI3K/Akt and PTEN pathway.
Insights
Baicalein (Bai) demonstrates neuroprotective effects against ischemic stroke by reducing infarct size and neuronal apoptosis. Its mechanism involves the PI3K/Akt and PTEN pathways, offering potential therapeutic benefits.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Emerging evidence suggests baicalein (Bai) possesses neuroprotective properties relevant to ischemic stroke.
- Understanding the precise molecular mechanisms underlying Bai's neuroprotection is crucial for therapeutic development.
Purpose of the Study:
- To elucidate the molecular pathways through which baicalein exerts its neuroprotective effects in models of ischemic stroke.
- To investigate the role of the PI3K/Akt and PTEN signaling pathways in Bai-mediated neuroprotection.
Main Methods:
- Middle cerebral artery occlusion (MCAO) was induced in rats to model ischemic stroke (permanent and transient).
- Primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic in vitro ischemic conditions.
- Levels of reactive oxygen species, nitrotyrosine, protein phosphorylation (Akt, GSK3beta, PTEN), and mitochondrial apoptotic markers were assessed.
- The effect of LY294002, a PI3K inhibitor, on Bai's protective effects was evaluated.
Main Results:
- Baicalein significantly reduced infarct volume and apoptosis in transient MCAO rats, but not permanent MCAO.
- Bai counteracted OGD-induced reactive oxygen species generation and neuronal injury in vitro.
- Bai restored OGD-impaired Akt and GSK3beta phosphorylation, associated with preserved PTEN phosphorylation.
- Bai increased Bcl-2/Bcl-xL-associated death protein phosphorylation and maintained mitochondrial Bcl-2 levels, inhibiting cytochrome c release.
- LY294002 blocked Bai-induced Akt phosphorylation and abolished its neuroprotective effect.
Conclusions:
- Baicalein exhibits significant neuroprotection against transient ischemic stroke in vivo and in vitro.
- The neuroprotective effects of baicalein are mediated through the PI3K/Akt signaling pathway, modulated by PTEN.
- These findings highlight baicalein as a potential therapeutic agent for ischemic stroke, acting via specific molecular pathways.
Related Concept Videos
00:49The Blood-brain Barrier
01:22Cerebral Edema ll: Pathophysiology