ArticleExperimental brain research2026
Parthenolide ameliorates bilirubin-induced neuronal cell injury by mediating autophagy.
Article in Experimental brain research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
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Authors and funding
4 authors.
Funding
Abstract
Unconjugated bilirubin (UCB) induces neurotoxicity in newborns, yet effective interventions remain limited. This study explores the neuroprotective role and mechanisms of parthenolide (PRT) using both in vivo and in vitro models. Primary rat neuronal cells exposed to UCB were evaluated through CCK-8, flow cytometry, Western blot, and immunofluorescence assays. Additionally, a rat model of bilirubin encephalopathy was established via bilirubin injection to verify PRT's effects in vivo. The results indicated that UCB significantly suppressed autophagy, increased LDH release and apoptosis, and reduced cell viability. PRT treatment effectively attenuated UCB-induced neuronal injury by enhancing autophagic activity. Mechanistically, PRT mediated these protective effects through inhibition of the AKT/mTOR pathway. These findings demonstrate that PRT exerts notable neuroprotective properties and may serve as a promising therapeutic candidate for bilirubin encephalopathy.
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Registered trials
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