ArticleFrontiers in neurology
Didymin mitigates neuroinflammation and preserves blood-brain barrier integrity after subarachnoid hemorrhage.
Article in Frontiers in neurology. 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
Objective: Subarachnoid hemorrhage (SAH) is a highly lethal and disabling type of stroke. The main causes of poor prognosis are neuroinflammation, blood-brain barrier (BBB) disruption and brain edema following hemorrhage. Didymin has shown neuroprotective effects in intracerebral hemorrhage; however, its regulatory role in SAH remains unclear. Methods: The rat SAH model was established using the internal carotid artery puncture method, while an Results: Didymin treatment significantly improved neurological function scores in SAH rats by alleviating neuronal damage and apoptosis. On one hand, didymin reduced post-SAH neuroinflammation by inhibiting excessive microglial activation and the expression of pro-inflammatory cytokines. On the other hand, didymin preserved BBB integrity and alleviated brain edema by downregulating MMP9 expression. In Hb-induced cell model, didymin suppressed MMP9 expression and promoted the expression of tight junction proteins. Conclusion: In this study, we demonstrated that didymin mitigates neuronal damage and apoptosis following SAH, effectively suppresses neuroinflammation, maintains the integrity of the BBB, and attenuates brain edema. These findings suggest that didymin holds promise as a potential therapeutic candidate for the treatment of SAH.
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