Wang G S, Liu G T
Department of Pharmacology, Chinese Academy of Medical Sciences, Beijing, China.
Zhongguo Yao Li Xue Bao. 1997 Mar;18(2):173-6.
To study the possible involvement of Kupffer cells (KC) in immunological liver injury in mice.
Liver injury was induced by i.v. injection of Bacillus Calmette-Guerin (BCG) 5 x 10(7) viable bacilli followed by i.v. injection of lipopolysaccharides (LPS) 7.5 micrograms to each mouse. Indian ink and silica were i.v. injected to suppress KC and retinol was given po to stimulate KC in these mice. Plasma alanine aminotransferase (AlaAT), aspatate aminotransferase (AspAT), nitric oxide (NO), and liver tissue were examined.
Injection of LPS following BCG injection resulted in a remarkable elevation of plasma NO, AlaAT, and AspAT levels, and severe liver damage. The damages were enhanced by the activation of KC with retinol and reduced by suppression of KC with silica and Indian ink.
The degree of liver injury induced by BCG + LPS is closely correlated with the status of KC, and NO from KC plays an important role in the pathogenesis of the liver damage in mice.
研究库普弗细胞(KC)在小鼠免疫性肝损伤中可能的作用。
通过静脉注射5×10⁷ 活芽孢的卡介苗(BCG),随后给每只小鼠静脉注射7.5微克脂多糖(LPS)诱导肝损伤。给这些小鼠静脉注射印度墨汁和二氧化硅以抑制KC,并口服视黄醇以刺激KC。检测血浆丙氨酸氨基转移酶(AlaAT)、天冬氨酸氨基转移酶(AspAT)、一氧化氮(NO)以及肝组织。
卡介苗注射后注射脂多糖导致血浆NO、AlaAT和AspAT水平显著升高,以及严重的肝损伤。视黄醇激活KC会加重损伤,而二氧化硅和印度墨汁抑制KC则会减轻损伤。
卡介苗+脂多糖诱导的肝损伤程度与KC的状态密切相关,KC产生的NO在小鼠肝损伤发病机制中起重要作用。