Kurebayashi Y, Ikeda T, Honda Y
Daiichi Pharmaceutical Co., Ltd., Tokyo, Japan.
Dig Dis Sci. 1992 May;37(5):645-9. doi: 10.1007/BF01296417.
16,16-Dimethyl prostaglandin E2 was examined for its ability to inhibit complement-mediated in vitro hepatocytolysis by an antigen-antibody reaction. In the presence of fresh rat serum as a source of complement, 5-min culture of isolated rat hepatocytes with a monoclonal antibody against a rat liver-specific membranous antigen resulted in a marked, significant elevation in lactate dehydrogenase leakage into the culture medium. However, with heat-inactivated rat serum, such a reaction did not occur, indicating that the hepatocytolysis induced by the antibody was attributable to the membrane damaging action of complement activated by an antigen-antibody reaction. Pretreatment of the hepatocyte with 16,16-dimethyl prostaglandin E2 significantly suppressed the cytolytic reaction induced by the antibody in a concentration-dependent manner. These results show that 16,16-dimethyl prostaglandin E2 is capable of protecting isolated rat hepatocytes against the membrane-damaging insult of activated complement.
研究了16,16 - 二甲基前列腺素E2抑制补体介导的体外抗原 - 抗体反应诱导的肝细胞溶解的能力。以新鲜大鼠血清作为补体来源，将分离的大鼠肝细胞与抗大鼠肝脏特异性膜抗原的单克隆抗体进行5分钟培养，导致培养基中乳酸脱氢酶泄漏显著明显升高。然而，使用热灭活的大鼠血清时，未发生这种反应，表明抗体诱导的肝细胞溶解归因于抗原 - 抗体反应激活的补体的膜损伤作用。用16,16 - 二甲基前列腺素E2预处理肝细胞以浓度依赖的方式显著抑制了抗体诱导的细胞溶解反应。这些结果表明，16,16 - 二甲基前列腺素E2能够保护分离的大鼠肝细胞免受活化补体的膜损伤侵害。
