摘要
采用胶原酶-链霉蛋白酶灌流法对免疫性肝损伤大鼠肝实质细胞与枯否细胞进行分离与原代培养，Griess反应法检测细胞培养上清中一氧化氮（NO）生成量的变化。结果显示在刺激条件及细胞数量同等情况下，肝实质细胞NO生成量显著高于枯否细胞；肿瘤坏死因子（TNFα）单克隆抗体可拮抗枯否细胞由细菌脂多糖（LPS）刺激所致NO生成的增加，而对卡介苗（BCG）所致NO生成无显著影响。提示免疫性肝损伤中NO生成主要源于肝实质细胞；LPS通过使枯否细胞释放TNFα对NO生成进行调节。
Using an in situ collagenase-pronase E perfusion technique, Kupffer's cells were isolated from hepatocytes in rat immunological hepatic injury, and nitric oxide (NO) production in culture supernatant was measured by the method of the Griess's reaction. The results indicated that NO production in hepatocytes was significantly higher than in Kuffer's cells under the similar stimulating conditions;TNFα-monoclonal antibody inhibited NO production induced by bacterial lipopolysaccharide (LPS) in Kupffer's cells, but did not affect that by stimulated bacille calmette guerin (BCG). These results implie that NO mainly originate from hepatocytes in rat immunological hepatic injury and LPS regulated NO production via promoting TNFα release in Kupffer's cells.
出处
《基础医学与临床》
CSCD
1999年第3期28-32,共5页
Basic and Clinical Medicine
基金
国家自然科学基金!39770861
关键词
免疫性
肝损伤
枯否细胞
一氧化氮合酶
immunological hepatic injury Kupffer's cells nitric oxide (NO)
