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Activated liver macrophages are considered to play an important role in the development of liver injuries. Functional differences between activated and normal rat liver macrophages were investigated. In addition, from the therapeutic point of view, the effects of prostaglandin E1, prostaglandin I2 and E3330 ((2E)-3-[5-(2,3-dimethoxy-6-methyl-1,4- benzoquinoyl)]-2-nonyl-2-propenoic acid) on the functions of liver macrophages were also determined. Rat liver macrophages were primed by Propionibacterium acnes and activated by a small dose of lipopolysaccharide. Lipopolysaccharide uptake capacity was evaluated quantitatively by flow cytometric analysis. Tumor necrosis factor-alpha activities were measured by bioassay. There were no significant differences in lipopolysaccharide uptake capacity between activated and normal liver macrophages, while activated liver macrophages had a significantly (P < 0.01) higher capacity in the release of tumor necrosis factor-alpha. Prostaglandin E1 and E3330 inhibited tumor necrosis factor-alpha release without suppressing lipopolysaccharide uptake capacity. In this study we have clarified the functional differences between activated and normal liver macrophages. The beneficial effects of prostaglandin E1 and E3330 on the functions of liver macrophages were also demonstrated.

To elucidate the differences in the progression of liver cirrhosis of chronic hepatitis B and C, the laparoscopic appearance of the liver surface and the histological findings were carefully assessed in 65 patients with chronic hepatitis B and 58 patients with chronic hepatitis C. There was a difference noted in the distribution of periportal reddish markings between the two types of chronic hepatitis. Localized and irregular markings were found to be common in hepatitis C. While the markings were seen to be diffusely distributed over the liver surface in hepatitis B. In addition, localized and longitudinal depressions on the liver surface were observbed more frequently in the hepatitis C patients than in those with hepatitis B. Biopsy specimens obtained from the hepatitis C patients with the above-mentioned laparoscopic findings showed more advanced histological activity. These laparoscopic changes developed in accordance with the progression of histological activity in chronic hepatitis C. Lymphoid follicles or aggregates within the portal areas were observed more frequently in the patients with chronic hepatitis C than in the chronic hepatitis B patients. Although it is not yet clear how the laparoscopic and histological differences between these two types of chronic hepatitis come about, it appears that the progression of hepatocellular necrosis in chronic hepatitis C is different from that of chronic hepatitis B.