Wang G, Liu G
Department of Pharmacology, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing.
Zhonghua Yi Xue Za Zhi. 1996 Mar;76(3):203-6.
To study the role of nitric oxide (NO) in mouse immunological liver injury.
Injection of either bacille calmette guréin (BCG) or lipopolysaccharide (LPS) alone in mice was used to induce moderate increase of plasma NO level and liver damage were seen after the
Administration of LPS following BCG injection resulted in remarkable elevation of plasma NO level and severe liver damage. The elevation of NO level and liver damage induced by BCG or BCG + LPS were not affected by administration of L-arginine, and substrate of NO synthase. Inhibition of NO synthase by NG-monomethyl-arginine (NMMA) decreased the elevated plasma NO without effect on the elevated plasma GPT and GOT levels induced by BCG injection. The BCG + LPS induced elevation of plasma GPT and GOT levels were more pronounced after NO production was inhibited by NMMA treatment. The action of NMMA mentioned above was partially reversed by simultaneous administration of L-arginine.
NO plays a protective action against liver injury induced by BCG + LPS in mice.
研究一氧化氮(NO)在小鼠免疫性肝损伤中的作用。
单独给小鼠注射卡介苗(BCG)或脂多糖(LPS)以诱导血浆NO水平适度升高,并观察之后出现的肝损伤情况。
在注射BCG后给予LPS导致血浆NO水平显著升高以及严重的肝损伤。BCG或BCG + LPS诱导的NO水平升高和肝损伤不受L - 精氨酸(NO合酶的底物)给药的影响。NG - 单甲基精氨酸(NMMA)抑制NO合酶可降低升高的血浆NO水平,但对BCG注射诱导的血浆谷丙转氨酶(GPT)和谷草转氨酶(GOT)水平升高没有影响。在通过NMMA处理抑制NO产生后,BCG + LPS诱导的血浆GPT和GOT水平升高更为明显。同时给予L - 精氨酸可部分逆转上述NMMA的作用。
NO对小鼠BCG + LPS诱导的肝损伤起保护作用。