ArticleLiver research (Beijing, China)2022
Protective effects of Longhu Rendan on chronic liver injury and fibrosis in mice.
Article in Liver research (Beijing, China), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Article
- Kehuang capsule inhibits MAPK and AKT signaling pathways to mitigate CClLiver research (Beijing, China) · 2024Article
- Application of mesenchymal stem cells in liver fibrosis and regeneration.Liver research (Beijing, China) · 2024Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and aim: Liver fibrosis resulting from persistent liver injury represents a major healthcare problem globally. Traditional Chinese medicine has played an essential role in the treatment of liver fibrosis in recent years. Thus, this study aims to assess the effect of Longhu Rendan (LHRD), a Chinese traditional patent medicine, on liver fibrosis and its potential mechanism. Methods: The liver fibrosis in mice was induced via the intraperitoneal injection of carbon tetrachloride (CCl Results: LHRD significantly suppressed the activity of serum index of abnormal liver function, liver cell apoptosis, and necrosis, attenuating liver injury. Moreover, LHRD treatment alleviated liver fibrotic features, such as the reduction of collagen deposition and hepatic stellate cell activation as well as profibrotic gene expression. Mechanistically, LHRD treatment inhibited nuclear transcription factor-kappa B signaling and inflammatory gene expression and diminished the production of reactive oxygen species and 4-hydroxynonenal, along with the downregulation of NADPH oxidase 4. Conclusions: Overall, the present study demonstrates that LHRD ameliorates liver injury and fibrosis via the inhibition of inflammation and oxidative stress in mice, indicating that LHRD is a potential medicine for the treatment of liver fibrosis.
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