ArticleFrontiers in neurology2024
Cynaroside: a potential therapeutic agent targeting arachidonate 15-lipoxygenase to mitigate cerebral ischemia/reperfusion injury.
Article in Frontiers in neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Nasal-to-Brain ROS-Responsive Diselenide-Bridged Graphene Nanogel for Targeted Ischemic Stroke Therapy via Microglial Modulation.ACS omega · 2026Article
- Ferroptosis in Ischemic Stroke: Insights from Natural Product Treatment and Future Directions.Drug design, development and therapy · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Due to the anti-inflammatory and antioxidant properties of cynaroside (Cyn), it may be useful in the treatment of cerebral ischemia/reperfusion injury (I/R). This study aims to evaluate the effect of Cyn on cerebral ischemia/reperfusion injury. Methods: Transient middle cerebral artery occlusion model (tMCAO) and oxygen and glucose deprivation/reperfusion (OGD/R) microglia models were used to evaluate the effect of Cyn. The direct interaction between Cyn and Alox15 was investigated through bioinformatics, molecular docking and biolayer interferometry. Results: tMCAO mice treated with Cyn show improved neurological deficits, reduced infarct volume and edema, and inhibition of microglial activation. In addition, Cyn inhibited tMCAO-induced Alox15 expression. Cyn significantly reduced the overproduction of the M1 microglia-regulated pro-inflammatory cytokines NLRP3, ASC, and cleaved caspase-1, as well as the overproduction of IL-1β and IL-18, induced by tMCAO or OGD/R. Cyn also inhibits the expression of Tfrc, COX2, and Acsl4 in tMCAO and OGD/R-treated mice and BV-2 cells. Discussion: These results suggest that Cyn may attenuate cerebral ischemia/reperfusion injury by inhibiting Alox15 to reduce inflammation and reduce ferroptosis. This study reveals the underlying molecular mechanism of Cyn in the treatment of ischemic stroke.
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