TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000407236
  • Gene Name:PPARA
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:RT-PCR
  • mRNA Pathway:PPAR signaling pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB01586
  • Drug Name:Ursodeoxycholic acid
  • Drug Method:up-regulated the gene expression

Disease basic infommation

  • Disease:hepatic fibrosis
  • Tissue:patients tissues

Other information

  • Title:Protective effect of cultured bear bile powder against dimethylnitrosamine-induced hepatic fibrosis in rats
  • Journal:Biomedicine & Pharmacotherapy
  • Published:2019
  • PubMed ID:30818137
  • Abstract:Natural bear bile has been used for liver disease in East Asia for thousands of years. However, its use has restrictions. In the current study, the therapeutic effects and potential mechanisms of cultured bear bile powder (CBBP) against hepatic fibrosis were evaluated in a dimethylnitrosamine (DMN)-induced rat model. CBBP treatment significantly improved DMN-induced hepatic necrosis and inflammatory infiltration. Additionally, CBBP remarkably alleviated the increased hepatic collagen content and expression of alpha-smooth muscle actin. Serum metabolomics revealed that 14 serum metabolites, including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were decreased in DMN-treated rats, which was reversed by CBBP. Pathway analyses revealed that the main metabolic pathways affected by CBBP were related to fatty acid biosynthesis and metabolism, and biosynthesis of unsaturated fatty acids. EPA and DHA are ligands of peroxisome proliferator activated receptors (PPARs). CBBP treatment significantly stimulated liver mRNA and protein expression of PPARα and PPARγ. CBBP also markedly increased liver expression of PPARα target genes, which are involved in fatty acid β-oxidation, and down-regulated IL-6, a downstream inflammatory gene of PPARγ. In conclusion, CBBP has the potential to attenuate liver fibrosis and its mechanism involves the promotion of the liver expression of PPARα and PPARγ. Our results may help in the development of a novel substitute for bear bile and therapeutic strategies for fibrotic liver diseases.
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