Baicalin Attenuates Ferroptosis after Subarachnoid Hemorrhage via the PI3K/AKT/GPX4 and NLRP3 Axis.

January 9, 2026

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Key Points

The research aims to explore how baicalin impacts ferroptosis after subarachnoid hemorrhage.
Investigate the effect of baicalin on ferroptosis in experimental models of subarachnoid hemorrhage.
Analyze the involvement of the PI3K/AKT pathway in this process.
Evaluate the role of NLRP3 in conjunction with GPX4 in ferroptosis modulation.
Baicalin significantly reduces indicators of ferroptosis after subarachnoid hemorrhage.
Activation of the PI3K/AKT pathway is observed with baicalin treatment.
NLRP3 and GPX4 levels are effectively regulated, supporting the protective role of baicalin.

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Research demonstrates baicalin alleviates ferroptosis after subarachnoid hemorrhage, suggesting a potential therapeutic approach.

Baicalin can alleviate ferroptosis after SAH by activating the PI3K/AKT pathway.

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Ling et al. (2026) studied this question.

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