Emergence of different macrophage populations in hepatic fibrosis following thioacetamide-induced acute hepatocyte injury in rats.

摘要: Macrophages may play a role in fibrogenesis. The kinetics and distribution of different macrophage populations were investigated immunohistochemically hepatic lesions following acute hepatocyte injury induced F344 rats by single injection thioacetamide (TAA) (300 mg/kg body weight, intraperitoneally). Hepatocyte degeneration or necrosis TAA occurred mainly the perivenular areas lobules as early post-injection (PI) days 1 3; fibrotic lesion development began damaged on day 1, peaked 5; thereafter (PI 7 10), decreased replaced regenerated hepatocytes PI 15 20, indicating remodelling process. In this rat model, number macrophages reacting with ED1 antibody (specific for exudate macrophages), ED2 (recognizing cell membrane antigens resident macrophages, including Kupffer cells) OX6 MHC class II expressed antigen-presenting dendritic to increase peaking 3. numbers gradually 5 7; however, statistically significant was maintained respect ED1-positive cells up whereas no ED2- OX6-positive remained from 10 onwards. Interestingly, ED1-, cells, least numerous. ED1- appeared exclusively injured areas, ED2-positive present mid-zonal smaller areas. These findings indicated differences between appearing fibrosis. addition, RT-PCR revealed that mRNA expression osteopontin, factor induction maintenance inflammation, markedly increased 5, 10, suggesting pathogenesis