Current neuropharmacology · 2026
A Review on the Molecular Mechanism Underlying the Protective Effect of Andrographolide Against Ischemic Stroke.
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Yuan Wei, Wei Haiping, Liu Jifei, Zhang Zhenchang
Аннотация
INTRODUCTION: Ischemic stroke (IS) is a major global health challenge, associated with high mortality and long-term disability. Current treatment strategies, including pharmacotherapy and acute reperfusion therapy, have significant limitations, underscoring the urgent need for novel neuroprotective agents. Andrographolide (AG), a bioactive compound derived from Andrographis paniculata, has demonstrated potent neuroprotective effects in various neurological disorders; however, the precise mechanisms underlying its efficacy in IS remain incompletely understood. This review aims to provide a comprehensive summary of the pharmacological effects of AG in IS, with the goal of identifying potential therapeutic avenues.
METHODS: A systematic literature search was conducted using PubMed, ScienceDirect, Web of Science, and Google Scholar, focusing on in vitro and in vivo studies that evaluated AG as a neuroprotective agent in the context of IS.
RESULTS: IS is a complex disease resulting from cerebral ischemia, which disrupts neural networks and triggers pathological processes including inflammation, blood-brain barrier (BBB) injury, and cell death. AG exhibits neuroprotective properties through multiple mechanisms, including antiinflammatory activity, endothelial cell protection, anti-apoptotic effects, and inhibition of platelet aggregation.
CONCLUSION: AG represents a promising neuroprotective candidate for IS, acting via diverse mechanisms and pathways. Further research is warranted to elucidate its molecular targets and to explore its clinical potential in IS therapy.
METHODS: A systematic literature search was conducted using PubMed, ScienceDirect, Web of Science, and Google Scholar, focusing on in vitro and in vivo studies that evaluated AG as a neuroprotective agent in the context of IS.
RESULTS: IS is a complex disease resulting from cerebral ischemia, which disrupts neural networks and triggers pathological processes including inflammation, blood-brain barrier (BBB) injury, and cell death. AG exhibits neuroprotective properties through multiple mechanisms, including antiinflammatory activity, endothelial cell protection, anti-apoptotic effects, and inhibition of platelet aggregation.
CONCLUSION: AG represents a promising neuroprotective candidate for IS, acting via diverse mechanisms and pathways. Further research is warranted to elucidate its molecular targets and to explore its clinical potential in IS therapy.