- 作者: Yi-Chao Hsu; Yung-Tsung Chiu; Chang-Yin Lee; Yun-Lian Lin; Yi-Tsau Huang
- 作者服務機構: Institute of Traditional Medicine, National Yang-Ming University School of Medicine, Taipei, Department of Education and Research, Taichung Veterans General Hospital, Taichung, and National Research Institute of Chinese Medicine, Taipei, Taiwan, ROC
- 中文摘要: --
- 英文摘要: Fibrosis-related changes in livers of cirrhotic rats in-duced by dimethylnitrosamine (DMN) have not yet beenfully clarified. The aim of this study was to investigatechanges in molecular and biochemical markers in DMN-intoxicated rats. DMN was administered to Sprague-Dawley rats for 2 and 5 weeks to induce different degreesof hepatic fibrosis. Liver tissues were assessed for thedegree of fibrosis and gene expression. Histological ex-amination of the liver showed a progressive increase infibrosis scores (1.33±0.21 and 3.03±0.29, respective-1y) and expansion of fibrous septa with collagen-stainingfibers in rats after 2 and 5 weeks of DMN administration.Hepatic protein contents of α-smooth muscle actin (α-SMA) and total collagen were significantly higher in ratsadministered DMN for both 2 and 5 weeks comparedwith those in control rats. Hepatic mRNA expressions ofα-SMA, transforming growth factor-β1 (TGF-β1), connec-tive tissue growth factor, tissue inhibitor of metallopro-teinase-1, and procollagen I and III were increased inDMN rats after 2 and 5 weeks. Abnormal increases inplasma alanine transaminase (ALT) and aspartate trans-aminase (AST) levels, plasma and mitochondrial MDAlevels, and portal venous pressure were also noted inDMN rats. DMN administration to rats for 2 and 5 weeksinduced progressive increases in hepatic fibrosis scores,hepatic mRNA expressions of TGF-β1 and procollagen Iand III genes, plasma levels of ALT and AST, and portalvenous pressure, as well as progressive decreases inboth liver and body weights. Our results suggest thatDMN administration in rats induces biochemical andmolecular changes related to fibrogenesis in the liver.
- 中文關鍵字: --
- 英文關鍵字: --