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Lodoxamide Attenuates Hepatic Fibrosis in Mice: Involvement of GPR35

PMID: 31189299 (view PubMed database entry)
DOI: 10.4062/biomolther.2018.227 (read at publisher's website )
PMCID: PMC6939691 (free full text version available)

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Mi-Jeong Kim, Soo-Jin Park, So-Yeon Nam, Dong-Soon Im,

A previous pharmacogenomic analysis identified cromolyn, an anti-allergic drug, as an effective anti-fibrotic agent that acts on hepatocytes and stellate cells. Furthermore, cromolyn was shown to be a G protein-coupled receptor 35 (GPR35) agonist. However, it has not been studied whether anti-fibrotic effects are mediated by GPR35. Therefore, in this study, the role of GPR35 in hepatic fibrosis was investigated through the use of lodoxamide, another anti-allergic drug and a potent GPR35 agonist. Longterm treatment with carbon tetrachloride induced hepatic fibrosis, which was inhibited by treatment with lodoxamide. Furthermore, CID2745687, a specific GPR35 antagonist, reversed lodoxamide-mediated anti-fibrotic effects. In addition, lodoxamide treatment showed significant effects on the mRNA expression of collagen Iα1, collagen Iα2, and TGF-β1 in the extracellular matrix. However, a transforming growth factor α (TGF-α) shedding assay revealed lodoxamide not to be a potent agonist of mouse GPR35 <i>in vitro</i>. Therefore, these results showed anti-fibrotic effects of lodoxamide in mice and raise concerns how lodoxamide protects against liver fibrosis <i>in vivo</i> and whether GPR35 is involved in the action.

Biomol Ther (Seoul) (Biomolecules & therapeutics)
[2019, :92-97]

Cited: 1 time

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