Interleukin-10 gene therapy reverses thioacetamide-induced liver fibrosis in mice

Kung Sheng Hung, Tsung Hsing Lee, Wen Ying Chou, Chia Ling Wu, Chung Lung Cho, Cheng Nan Lu, Bruno Jawan, Cheng Haung Wang

Research output: Contribution to journalArticlepeer-review

56 Citations (Scopus)


Hepatic fibrosis represents a process of healing and scarring in response to chronic liver injury. Interleukin-10 (IL-10) is a cytokine that downregulates the proinflammatory response and has a modulatory effect on hepatic fibrogenesis. The aim of this study was to investigate whether IL-10 gene therapy possesses anti-hepatic fibrogenesis in mice. Liver fibrosis was induced by long-term thioacetamide administration in mice. Human IL-10 expression plasmid was delivered via electroporation after liver fibrosis established. IL-10 gene therapy reversed hepatic fibrosis and prevented cell apoptosis in a thioacetamide-treated liver. RT-PCR revealed IL-10 gene therapy to reduce liver transforming growth factor-β1, tumor necrosis factor-α, collagen α1, cell adhesion molecule, and tissue inhibitors of metalloproteinase mRNA upregulation. Following gene transfer, the activation of α-smooth muscle actin and cyclooxygenase-2 was significantly attenuated. In brief, IL-10 gene therapy might be an effective therapeutic reagent for liver fibrosis with potential future clinical applications.

Original languageEnglish
Pages (from-to)324-331
Number of pages8
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - Oct 14 2005
Externally publishedYes


  • COX-2
  • Gene therapy
  • IL-10
  • Liver fibrosis
  • Thioacetamide

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry
  • Cell Biology


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