Article3 Biotech2026
Gandouling protects against hepatic fibrosis in Wilson disease through the lncRNA-SNHG7/miR-29b/DNMT3A pathway.
Article in 3 Biotech, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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8 authors.
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Abstract
The therapeutic efficacy of Gandouling (GDL) against hepatic fibrosis, along with its underlying mechanisms, was evaluated in a model of Wilson disease (WD). Using a copper-loaded rat model and in vitro LX-2 cell assays, we comprehensively evaluated the effects of GDL by employing transmission electron microscopy (TEM), histopathology, ultrasound elastography, confocal microscopy (mCherry-GFP-LC3 assay), qRT-PCR, and Western blotting. GDL treatment significantly improved liver function, indicated by reduced serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronic acid (HA), laminin (LN), type III pre-collagen (PC-III), and collagen IV (C-IV). GDL also reduced the hepatic copper content and ameliorated histopathological and ultrasonographic signs of fibrosis. At the molecular level, GDL downregulated the expression of lncRNA SNHG7, DNMT3A, α-smooth muscle actin (α-SMA), and collagen I, while upregulating the expression of miR-29b. Furthermore, GDL inhibited autophagy, as shown by reduced levels of Beclin-1 and LC3-II/LC3-I and decreased autophagosome formation. These results demonstrate that GDL alleviates copper overload-induced hepatic fibrosis through modulation of the SNHG7/miR-29b/DNMT3A axis and inhibition of excessive autophagy.
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