Enzan H
Acta Pathol Jpn. 1987 Feb;37(2):225-30. doi: 10.1111/j.1440-1827.1987.tb03058.x.
Small tissue blocks of livers obtained from normal and CCl4-treated mice were incubated in culture medium supplemented with 3H-leucine for one hour to observe the protein synthesis of Ito cells in acute carbon tetrachloride liver injury by a light and electron microscopic autoradiography. In normal mouse liver very few Ito cells are labeled with 3H-leucine. On the contrary, in acutely damaged mouse liver by a single intraperitoneal injection of CCl4, the Ito cells in the centrilobular zones where liver cells show marked degeneration and necrosis are densely labeled. No labeling, however occurs over the Ito cells in the intermediate and peripheral zones of the same liver lobules, where liver cells showed no cellular degeneration. These findings show that the Ito cells are inactive in 3H-leucine incorporation under physiological conditions. After acute liver cell injury the Ito cells located in the necrotic areas of liver cells are markedly activated for protein synthesis.
从正常小鼠和四氯化碳处理的小鼠获取小块肝脏组织,将其在补充有3H-亮氨酸的培养基中孵育一小时,通过光镜和电镜放射自显影观察急性四氯化碳肝损伤中贮脂细胞的蛋白质合成。在正常小鼠肝脏中,极少有贮脂细胞被3H-亮氨酸标记。相反,在通过单次腹腔注射四氯化碳造成急性损伤的小鼠肝脏中,肝细胞呈现明显变性和坏死的小叶中心区的贮脂细胞被密集标记。然而,在同一肝小叶的中间区和周边区的贮脂细胞上没有标记,这些区域的肝细胞未显示细胞变性。这些发现表明,在生理条件下贮脂细胞在3H-亮氨酸掺入方面不活跃。急性肝细胞损伤后,位于肝细胞坏死区域的贮脂细胞在蛋白质合成方面被显著激活。