Figure 3
From: IGF-I induces senescence of hepatic stellate cells and limits fibrosis in a p53-dependent manner
IGF-I treatment decreased the marker of activated HSCs in NASH model mice and improved hepatic fibrosis in cirrhosis model mice.
(a) Immunohistological analysis of αSMA, which is an activated marker for HSCs in control or IGF-I-treated NASH model mice (n = 5 for each groups). (b) Quantitative analysis of αSMA-positive cells in the liver. (c) Quantitative realtime PCR analysis reveals decreased expression of HSCs marker (αsma and Vimentin) and Timp-1 and increased expression of Mmp9 in the IGF-I-treated liver. (d) Immunofluorescence analysis for double staining of αSMA and IGF-I receptor (IGF-IR) showed a co-localization in HSCs (800×). (e) The treatment with IGF-I in DMN-induced cirrhotic mice model (n = 5 for each groups). Human recombinant IGF-I or vehicle were administered cirrhotic mice using osmotic pump for 6 weeks. Sirius Red staining visualized the fibrosis of the liver (100×). Quantification of fibrosis based on Sirius Red staining. Fibrotic area was significantly decreased by IGF-I in DMN-induced cirrhotic mice. (f) Quantitative realtime PCR analysis revealed the decreased expression of αsma, Vimentin, and Timp1 and increased expression of Mmp9 by IGF-I treatment.
