ArticleFrontiers in pharmacology2026
Baicalin-geniposide attenuates pulmonary inflammation and vascular injury via HMGB1 blockade: insights from a cerebral ischemia-reperfusion model and implications for pulmonary hypertension.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The active role of pulmonary immunity in ischaemic stroke.Journal of neuroinflammation · 2026Review
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5 authors.
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Abstract
Introduction: Pulmonary complications following stroke are a leading cause of death, with no targeted therapies available. Inflammation drives both post-stroke neurological damage and secondary acute lung injury (CIS-ALI). High mobility group box 1 (HMGB1), a key mediator in cerebral ischemia stroke (CIS), translocates from the nucleus to cytoplasm and is released extracellularly, triggering inflammatory cascades. The combination of two bioactive metabolites, baicalin and geniposide (BG), exhibits anti-inflammatory and neuroprotective properties, but its efficacy against CIS-ALI remains unexplored. This study investigated BG's mechanisms using Methods: This study investigated the mechanisms of BG using Results: BG dose-dependently suppressed pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and nitric oxide (NO), while attenuating HMGB1 nucleocytoplasmic translocation via JAK2/STAT3 inhibition. BG (25-50 mg/kg) reduced cerebral infarct volume, neurological deficits, and lung edema. Mechanistically, BG blocked HMGB1 nuclear export in ischemic brains, thereby decreasing HMGB1 levels in serum and lungs, and disrupting inflammatory cross-talk. Discussion: These findings highlight BG's unique capacity to concurrently mitigate cerebral injury and secondary ALI by targeting the JAK2/STAT3 axis, offering a safe, multi-targeted strategy against CIS-related complications. Given the shared pathological features between ALI and PH-including inflammation, vascular hyperpermeability, and JAK2/STAT3-driven injury cascades-these findings provide a mechanistic rationale for exploring BG as a potential therapeutic candidate for pulmonary hypertension and related pulmonary vascular diseases.
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