ArticleMetabolic brain disease2025
Hydroxysafflower yellow A alleviates the inflammatory response in astrocytes following cerebral ischemia by inhibiting the LCN2/STAT3 feedback loop.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Secondary demyelination after stroke: Glial cell crosstalk.IBRO neuroscience reports · 2026Review
- Hydroxysafflor yellow a attenuates oxygen-glucose deprivation/ reoxygenation induced endothelial pyroptosis via PARP-1/NLRP3 pathway.Frontiers in pharmacology · 2026Article
- Neuroprotective potential of indian herbs in ischaemic stroke: a comprehensive review of pharmacological insights, therapeutic gaps, and future directions.Inflammopharmacology · 2025Review
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12 authors.
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Abstract
Lipocalin-2 (LCN2), an acute phase protein mainly expressed in astrocytes (Ast), is closely related to the production of inflammatory cytokines following ischemic stroke. During the pathophysiological process of ischemic stroke, the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway is activated. Despite evidence suggesting some link between the two, the relationship between the JAK2/STAT3 signaling pathway and the LCN2 expression in Ast following brain ischemia is incompletely understood. Hydroxysafflower yellow A (HSYA), an active ingredient found in Carthamus tinctorius L flowers, has been demonstrated to effectively mitigate cerebral ischemia via its anti-inflammatory effect. However, whether HSYA mitigates the neuroinflammatory damage after ischemic stroke by disrupting the interaction between the JAK2/STAT3 signaling pathway and LCN2 in Ast is unknown. Focusing on these two scientific questions, we established an in vivo middle cerebral artery occlusion/reperfusion (MCAO/R) rat model and in vitro primary astrocyte oxygen glucose deprivation/reperfusion (OGD/R) model. In vivo results showed that HSYA treatment alleviated nerve damage and inhibited the expression of LCN2 and inflammatory factors in Ast. In vitro results showed after OGD/R the expression of LCN2 and inflammatory cytokines increased and the JAK2/STAT3 was activated in Ast. Meanwhile, after OGD/R the JAK2/STAT3 activation in Ast increased LCN2 expression, and the inhibition of LCN2 expression by HSYA decreased the JAK2/STAT3 activation in Ast. These findings suggest that there is an interaction between the LCN2 and JAK2/STAT3 in Ast after ischemic stroke, which can enhance the inflammatory factors and exacerbate neuroinflammatory injury. Therefore, we conclude that HSYA may inhibit the LCN2/STAT3 loop in Ast, thereby mitigating neuroinflammation after cerebral ischemia.
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