ArticleFrontiers in pharmacology2025
Hypericin alleviates cerebral ischemia/reperfusion injury by modulating endoplasmic reticulum stress.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Cerebral ischemia/reperfusion (I/R) injury remains a leading cause of neurological disability and is characterized by oxidative stress, calcium overload, inflammation, and endoplasmic reticulum (ER) stress following reperfusion. Hypericin, a bioactive naphthodianthrone derived from Hypericum perforatum, exhibits antioxidant and anti-apoptotic properties. This study investigated the neuroprotective effects and underlying mechanisms of hypericin in experimental cerebral I/R injury. Methods: Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) and treated intraperitoneally with hypericin (5, 10, or 20 mg/kg) 30 minutes before reperfusion or nimodipine (10 mg/kg) as a positive control. Neurological severity scores (mNSS), grip strength, rotarod performance, infarct volume, and brain water content were evaluated 24 hours after reperfusion. Results: Hypericin significantly reduced cerebral infarct volume by approximately 40%, alleviated brain edema, and improved neurological and motor function compared with untreated I/R animals (p < 0.05). Histopathological and immunohistochemical analyses demonstrated preserved hippocampal structure and reduced caspase-3 activation. In OGD/R-injured HT22 cells, hypericin increased cell viability, reduced apoptotic rates from 30.3% to 10.3%, suppressed ER stress-associated markers (CHOP, GRP78, caspase-12), and normalized the Bax/Bcl-2 ratio. Pharmacokinetic predictions suggested moderate lipophilicity and physicochemical properties compatible with partial blood-brain barrier penetration, particularly under ischemia-induced barrier disruption. Discussion: These findings demonstrate that hypericin confers significant neuroprotection against cerebral I/R injury by attenuating ER stress-mediated apoptosis and preserving neuronal integrity. Hypericin may represent a promising therapeutic candidate for ischemic stroke.
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