ArticleAnnals of translational medicine2022
Methyltransferase SETD2 mediates hepatoprotection of berberine against steatosis.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Berberine Effects in Pre-Fibrotic Stages of Non-Alcoholic Fatty Liver Disease-Clinical and Pre-Clinical Overview and Systematic Review of the Literature.International journal of molecular sciences · 2024Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Berberine (BBR) can alleviate nonalcoholic fatty liver (NAFL), but the mechanisms remain uncertain. Mounting evidence has underscored the roles of epigenetic modulation in the development of NAFL. Increased expression of histone methyltransferase SET domain-containing protein 2 (SETD2) is found in the livers of diabetic animals with BBR administration. Whether SETD2 contributes to the protective effects of BBR against NAFL remains to be elucidated. Methods: A C57BL/6 mouse model of NAFL induced by a high-fat high-sucrose diet (HFHS) and a palmitate-treated hepatocyte steatosis model were generated. The effects of BBR were evaluated by Oil Red O staining and the cell viability assay. Quantitative real-time polymerase chain reaction, Western blotting, and immunofluorescence staining were used to analyze the expression and activity of SETD2 and its downstream target trimethylation of lysine 36 on histone 3 (H3K36me3). Results: BBR treatment induced the reduction of lipid droplets in both HFHS mouse livers and HepG2 cells, coincident with the elevation of the mRNA and protein expression of SETD2 and H3K36me3. Knockdown of SETD2 compromised the BBR-mediated inhibition of the accumulation of lipid droplets in the HepG2 cell model of steatosis. Moreover, upregulated SETD2 and H3K36me3 expression was also observed in intact HepG2 cells treated with BBR. The promoter assay indicated that BBR treatment increased the transcriptional activity of SETD2 and H3K36me3. Conclusions: BBR confers hepatoprotection against steatosis through transcriptional regulation of SETD2 activity.
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Registered trials
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