ArticleNeurochemical research2025
Ciwujianoside C Attenuates Cerebral Ischemia-Reperfusion Injury by Suppressing Ferroptosis via NNAT-Mediated Inhibition of NF-κB Signaling.
Article in Neurochemical research, 2025. 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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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
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia-reperfusion injury (CIRI) involves oxidative stress, inflammation, and regulated cell death, among which ferroptosis has emerged as a key contributor. However, therapeutic strategies targeting ferroptosis remain limited. This study investigated whether Ciwujianoside C (CC), a triterpenoid saponin from Acanthopanax senticosus, protects against CIRI by modulating ferroptosis via the NNAT/NF-κB pathway. In MCAO/R rats, CC reduced infarct size, improved neurological scores, and ameliorated oxidative stress and ferroptosis markers. In BV2 microglia and HT22 cells (a mouse hippocampal neuronal cell line) subjected to OGD/R, CC enhanced cell viability, decreased iron accumulation, and restored GPX4 and FTH1 expression while inhibiting NF-κB activation. Importantly, NNAT knockdown abolished these protective effects, demonstrating NNAT as a critical mediator. These findings reveal that CC protects against CIRI by suppressing ferroptosis through the NNAT/NF-κB axis, highlighting NNAT as a potential therapeutic target in CIRI.
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Registered trials
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