背景和目的：缺血的肝組織恢復再灌流後會產生氧化壓力及氮化壓力，因而造成去氧核醣核酸股之斷裂，以致活化了聚核醣二磷酸形成?，造成核內輔? NAD+及三磷酸腺?酸之消失，引起不可逆之細胞毒性。本研究中我們證實聚核醣二磷酸形成?抑制劑3-胺基苯醯胺可減輕缺血/再循環造成之肝損傷。方法：缺血是透過將肝總動脈及門靜脈夾住40 分鐘，然後再恢復灌流90 分鐘。缺血前及再循環後均抽血以分析血中一氧化氮及甲基胍含量變化而肝損傷指數則以AST 和ALT 當作指標。結果：此結果證實肝缺血再循環會造成一氧化氮之上升(p < 0.01) 而表示發炎反應之甲基胍也明顯的增加(p < 0.001)。肝功能指數AST 及ALT 也增加4～5 倍(p < 0.001)。當給予3-胺基苯醯胺(20mg/kg) 後肝損傷明顯地減弱而一氧化氮及甲基胍也一併減少。結論：此研究結果說明3-胺基苯醯胺可透過多種的功能產生抗發炎效果因而減少肝損傷。

Background and Purpose: Reperfusion of an ischemic liver results in the generationof oxidative stress and nitrosative stress, both of which can cause strand breaks in DNA,thus activating nuclear enzyme poly (ADP-ribose) synthase (PARS). This results in rapiddepletion of intracellular NAD+ and ATP and eventually induces irreversible cytotoxicity.In this study, we demonstrate that a PARS inhibitor, 3-aminobenzamide, attenuatedischemia/reperfusion (I/R)-induced liver injury. Methods: Ischemia was induced byclamping the common hepatic artery and portal vein of rats for 40 min. Thereafter, flowwas restored, and the liver was reperfused for 90min. Blood samples collected prior to theischemia and after the reperfusion were analyzed for methyl guanidine (MG), NO, andwhite blood cells. Blood levels of aspartate transferase (AST) and alanine transferase(ALT), which serve as indices of liver injury, weremeasured. Results: Results showed thatthis protocol resulted in elevation of the blood NO level (p < 0.01). Inflammation wasapparent, as white cells andMGlevels were significantly increased (p < 0.05 and p < 0.001,respectively). AST and ALT were elevated to 4~5-fold of their respective baselines (both p< 0.001). After administration of 3-aminobenzamide (20 mg/kg), liver injury wassignificantly attenuated while MG (p < 0.001) and NO (p < 0.05) releases were reduced.Conclusion: These results indicate that 3-aminobenzamide, presumably by acting throughmultiple functions, exerts potent anti-inflammatory effects in I/R-induced liver injury.