Ultrastructural changes of fat-storing cells in experimental hepatic fibrosis / 영남의대학술지

Hepatic fibrosis was induced in Sprague-Dawley rate to evaluate the ultrastructural changes of fat-storing cells (Ito cells). For experimental induction of liver fibrosis, the rats were administered intraperitoneally with 0.5 ml of 50% Ccl4 solution per Kg body weight, twice weekly for 12 weeks. The rats were sacrificed every week. The liver tissues were examined under light and electron microscopes. And the immunohistochemical study of desmin was also performed. The results were summarized as follows: Light microscopic findings: The cellular infiltrations was inflammatory cells and Kupffer cells developed from 1 week after Ccl4 injection, and were the most severe in 4 weeks. The strong immunoreactivity for desmin was also evident in 4 weeks. The centrilobular necrosis and fibrosis developed from 2 weeks after injection, and the necrosis persisted until 8 weeks. The progress of fibrosis was accompanied by decreases in cellular infiltration and reactivity for desmin, and increased gradual nodular formation was also observed. The cirrhosis was developed after 10 weeks. Electron microscopic findings: An increase in number of fat-storing cells was observed from 1 week after injection. Transitional cells characterized by a depletion of lipid droplets and a hypertrophy of the rER appeared after 2 weeks. The number of transitional cells with abundant collagen fibers in the extracellular spaces increased in 4 weeks. With progression of fibrosis the number of fat-strong cells decreased and proliferating fibroblasts with dilated rER were observed. According to these results it was revealed that there was an apparent transition from fatstrong cells to transitional cells and to fibroblasts. These cells had a few similar characteristics and may belong to the same cell population. Thus it was suggested that fatstrong cells might play an important role in hepatic fibrosis.

Ultrastructural Dynamic Observation on Murine Schistosomal Hepatic Fibrosis / 中国寄生虫学与寄生虫病杂志

Objective To explore possible mechanisms of hepatic fibrosis by investigating the ultrastructural dynamic changes of liver tissue, especially several kinds of cells related to hepatic fibrosis.. Methods. Murine schistosomal hepatic fibrosis model was established by infecting mice with Schistosoma japonicum cercariae. Routine transmission electron microscopy was used to observe the liver tissue. H.E. staining was used for examining the pathological changes. . Results . H.E. staining showed that the model was established successfully. Ultrastructural observation showed that at the 6th week after infection, the necrosis of hepatocytes around the acute granulomas occurred; the number of sinusoidal endothelial fenestrae and vitamin A droplets in fat-storing cells decreased; large phagosomes and rough endoplasmic reticulum could be seen in the cytoplasm of Kupffer′s cells. At the 8th week, steatosis was found in some hepatocytes, some microvilli emerged on a few inter-hepatocytic surfaces and the inter-hepatocytic spaces were enlarged. Large collagen fibrillar bundles filled in the perisinusoidal spaces, and capillarization of hepatic sinusoids was observed. Secretory vesicles filled with collagen fibrils appeared in the cytoplasm of fat-storing cells with large amount of collagenous fiber bundles surround the cells. Rough endoplasmic reticulum increased in Kupffer′s cells. At the 10th week, fat-storing cells were activated and transformed into myofibroblasts. At the 12th week, the number of myofibroblasts decreased but that of fibroblasts and fiber cells increased. . Conclusion . Activation of fat-storing cells and transformation from fat-storing cells into myofibroblasts are the critical link in the development of hepatic fibrogenesis following schistosome infection. Kupffer′s cells, necrotic hepatocytes and sinusoidal endothelial cells may relate to the activation of fat-storing cells. Capillarization of hepatic sinusoids possibly accelerates the development of hepatic fibrosis.

ULTRASTRUCTURE OF THE DEVELOPMENT OF HEPATIC FAT-STORING CELL IN RAT EMBRYO / 解剖学报

The ultrastructure of hepatic fat-storing cells in rat embryos was investigatedwith transmission electron microscope.It is considered that the rat fat-storingcells originate from mesenchymal cells.As the embryo develops,the fat-storing cell decreases in size gradully,this isespecially obvious at the time of birth.This may be related with the function of thistype of cell.In the hepatic fat-storing cell in embryo of 10 to 12 days,the roughendoplasmic reticulum has developed,the cell is rich in free ribosomes,and collagenfibrils may be observed in Disse's spaces.This indicates that the fat-storing cellshave possessed the function of synthesizing collagen.In embryo of 13 to 15 days,fat droplets appear in a few fat-storing cells and smooth endoplasmic reticulum, glycogen granules and pinocytosis may be seen at this time.It is suggested that thefunction of the uptake and storage of vitamin A may appear at that time too.There are desmosomes between the fat-storing cell and the hepatocyte.On the 16to 18 days,desmosomes are also present between the fat-storing cell and endothelialcell.This indicates that fat-storing cells are not free cells,but are bound to hepa-tocytes and endothelial cells via cellular junctions,At that time,microfilaments andmicrotubules are found in fat-storing cells,they are the skeleton of the cells andthey may be related to the regulation of the size of the sinusoids.In thedevelopment of embryo,the number of fat-storing cells and fat droplets have notincreased markedly,therefore,it is thought that they are increased after birth.