ArticleChinese medicine2025
Dendrobine alleviates CCl
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Merits of bioactivity and products ofFrontiers in plant science · 2026Pooled it
- Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundAcute liver injury (ALI) represents a critical clinical challenge characterized by rapid degradation of hepatic function, necessitating prompt intervention for improved patient outcomes. Dendrobine (DDB) is the main bioactive component of Dendrobium nobile Lindl. (DNL), a traditional Chinese herb renowned for its protective effects against liver injury. However, the specific mechanisms underlying its hepatoprotective effects have not yet been fully elucidated.
objectiveThis study aims to elucidate the potential mechanism underlying the protective effects of DDB against ALI, particularly through the Nrf2/PPARγ/SOD2 pathways, to provide a scientific basis for its application in ALI treatment.
methodsCCl
resultsDDB effectively suppressed MLKL activation and significantly alleviated ALI. DDB also upregulated Nrf2/PPARγ/SOD2 expression and reduced mtROS production. Further studies using pharmacological approaches showed that PPARγ activation increased SOD2 expression, reduced p-MLKL, and lowered mtROS levels. Conversely, PPARγ inhibition reversed these effects and diminished DDB's efficacy. Silencing Nrf2 in vivo decreased PPARγ/SOD2 expression and activated MLKL, counteracting DDB's protective effects. Overexpression of Nrf2 prevented the decrease in PPARγ/SOD2 protein expression induced by CCl
conclusionThis study demonstrates that DDB inhibits mtROS and p-MLKL through the Nrf2/PPARγ/SOD2 signaling axis, thereby suppressing necroptosis and ameliorating ALI.
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Registered trials
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