Muriel P, González P
Departamento de Farmacología y Toxicología, Centro de Investigación y de Estudios Avanzados del I.P.N., Mexico, D.F., Mexico.
Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1998 Oct;120(3):421-4. doi: 10.1016/s0742-8413(98)10018-x.
The aim of this paper was to determine if NO modulation would influence liver damage induced by 3 day-biliary obstruction. L-Arginine (500 mg kg-1, p.o. twice a day) or L-NAME (100 mg kg-1, p.o. twice a day) or both were administered to male Wistar rats subjected to bile duct ligation (BDL). In the liver, BDL doubled lipid peroxidation and depleted glycogen (P < 0.05), L-arginine completely prevented the former and partially the latter. Alkaline phosphatase, alanine aminotransferase and gamma-glutamyl transpeptidase serum enzyme activities increased (P < 0.05) by BDL, again L-arginine treatment partially, but significantly, prevented the elevation in these three markers of liver damage. Although L-NAME treatment failed to induce a change in any marker of liver injury studied herein, it abolished the beneficial effects of L-arginine, suggesting that these effects are probably mediated by NO synthesis stimulation.
本文旨在确定一氧化氮（NO）调节是否会影响3日胆道梗阻诱导的肝损伤。将L-精氨酸（500mg/kg，口服，每日两次）或L-硝基精氨酸甲酯（L-NAME，100mg/kg，口服，每日两次）或两者给予接受胆管结扎（BDL）的雄性Wistar大鼠。在肝脏中，BDL使脂质过氧化增加一倍并耗尽糖原（P<0.05），L-精氨酸完全阻止了前者，部分阻止了后者。碱性磷酸酶、丙氨酸转氨酶和γ-谷氨酰转肽酶血清酶活性因BDL而增加（P<0.05），L-精氨酸治疗再次部分但显著地阻止了这三种肝损伤标志物的升高。尽管L-NAME治疗未能引起本文研究的任何肝损伤标志物的变化，但它消除了L-精氨酸的有益作用，表明这些作用可能是由NO合成刺激介导的。
