Mizoguchi Y, Kuboi H, Kodama C, Sakagami Y, Seki S, Kobayashi K, Yamamoto S, Morisawa S
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Gastroenterol Jpn. 1987 Dec;22(6):743-7. doi: 10.1007/BF02776748.
When heat-killed Propionibacterium acnes (P. acnes) and a small amount of endotoxin lipopolysaccharide (LPS) were intravenously injected into mice at a week's interval, most of them died of massive hepatic cell necrosis. This experimentally-induced acute liver injury was significantly inhibited by cyclosporin A (CsA), resulting in a remarkable improvement of the survival rate. This protective effect of CsA on acute liver injury was also histopathologically confirmed. To study the mechanism by which CsA protected the mice from fatal hepatic injury, adherent cells prepared from the murine liver 7 days after P. acnes injection were incubated with LPS in the presence of CsA, and the effect of CsA on the production of the cytotoxic factor from the adherent cells was estimated. As a result, CsA inhibited the activation of liver adherent cells and suppressed the release of the cytotoxic factor.
当以一周的间隔向小鼠静脉注射热灭活痤疮丙酸杆菌（P. acnes）和少量内毒素脂多糖（LPS）时，大多数小鼠死于大规模肝细胞坏死。这种实验诱导的急性肝损伤被环孢素A（CsA）显著抑制，导致存活率显著提高。CsA对急性肝损伤的这种保护作用也得到了组织病理学证实。为了研究CsA保护小鼠免受致命性肝损伤的机制，在注射P. acnes 7天后从小鼠肝脏制备贴壁细胞，在CsA存在的情况下将其与LPS一起孵育，并评估CsA对贴壁细胞细胞毒性因子产生的影响。结果，CsA抑制了肝贴壁细胞的活化并抑制了细胞毒性因子的释放。
