Miyajima T, Kotake Y
National Biomedical Center for Spin Trapping and Free Radicals, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA.
Biochem Biophys Res Commun. 1995 Oct 4;215(1):114-21. doi: 10.1006/bbrc.1995.2440.
Spin trapping agent, phenyl N-tert-butyl nitrone (PBN) significantly reduces mortality due to lipopolysaccharide (LPS)-induced shock in Balb/c mice as had previously been shown in rats. We hypothesized that PBN decreases mortality by directly or indirectly inhibiting nitric oxide (NO) generation. Therefore, we determined the effect of PBN administration on LPS-induced NO generation in mice. NO generation was monitored in the mouse liver after administration of LPS by an in vivo NO-spin trapping, followed by ex vivo EPR measurement. When the mice was treated with PBN 0.5hr before LPS administration, NO generation in the liver was reduced by 80%. However, when PBN was given 3hrs after LPS, NO generation did not change. Both pre- or post-administration of NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine inhibited the NO generation. Western blotting of inducible NOS (iNOS) in mouse liver cytosol obtained from PBN-pretreated animals demonstrated a decreased expression of iNOS, indicating the reduction in NO generation was caused by the decrease in the amount of enzyme present but not by the inhibition of iNOS enzyme activity per se.
自旋捕捉剂苯基叔丁基硝酮(PBN)能显著降低脂多糖(LPS)诱导的Balb/c小鼠休克死亡率,此前在大鼠中也有类似发现。我们推测PBN通过直接或间接抑制一氧化氮(NO)生成来降低死亡率。因此,我们测定了给予PBN对LPS诱导的小鼠NO生成的影响。通过体内NO自旋捕捉,随后进行体外电子顺磁共振测量,监测LPS给药后小鼠肝脏中的NO生成。当在给予LPS前0.5小时用PBN处理小鼠时,肝脏中的NO生成减少了80%。然而,当在LPS给药后3小时给予PBN时,NO生成没有变化。一氧化氮合酶(NOS)抑制剂NG-单甲基-L-精氨酸的给药前或给药后均抑制了NO生成。对PBN预处理动物的小鼠肝脏细胞质中的诱导型NOS(iNOS)进行蛋白质印迹分析,结果显示iNOS表达降低,这表明NO生成减少是由于酶含量的减少,而不是iNOS酶活性本身受到抑制所致。