中文摘要：

瞄准：探索共同释放的效果分子[tricarbonyldichlororuthenium (II ) 更暗淡， CORM-2 ] 在一个实验动物的肝的煽动性的回答的变细上的解放公司热损害并且到当模特儿调查联系潜在的机制。方法：36 只老鼠在三个各自的实验被分到三个组。在每个实验，在假冒的组的鼠标( n = 4 )收到的假冒的热损害，而在灼伤的鼠标组织( n = 4 )收到了15%全部的身体表面区域( TBSA )完整厚度的热损害，并且在灼伤+ CORM-2 的鼠标组织( n = 4 )与 CORM-2 的立即的管理收到了一样的热损害( 8 mg/kg ， iv )。肝的织物节与苏木精和曙红被染色并且在一台轻显微镜下面检验了。aminotransferases (中高音和著名计算机生产厂商) 和氮的氧化物的层次(没有) 被生物化学的方法测量。肿瘤坏死 factor-alpha (TNF-alpha ) 和 interleukin (IL-1beta ) 活动，和在浆液和织物 homogenates 的 i NOS 和 HO-1 的蛋白质表示被估计。在在试管内实验， Kupffer 房间当面为 4 h 与 LPS (10 mug/mL ) 被刺激或 CORM-2 (10-100 mumol/L ) 的缺席。随后， TNF-alpha 的表示层次和没有生产被估计。结果：支持 inflammatory 调停人(TNF-alpha， IL-1beta，没有) 在浆液和肝，热地受伤的老鼠的 homogenates 被 CORM-2 管理显著地减少。这被减少在 i NOS 的表示伴随当时在肝织物的 HO-1 的表示的增加。在平行，在刺激 LPS 的 Kupffer 房间的上层清液的 TNF-alpha 并且不的集中与 CORM-2 (10-100 mumol/L ) 共同孵化显著地也被减少。组织学的检查证明 CORM-2 能稀释白血球渗入到肝织物。结论：释放球茎的公司调制肝发炎并且显著地由禁止 i NOS 和没有生产的表示在灼伤老鼠保护肝损伤，下面调整支持 inflammatory 调停人的表示(TNF-alpha， IL-1beta ) 。

英文摘要：

AIM： To explore the effects of CO-releasing molecules [tricarbonyldichlororuthenium （Ⅱ） dimer, CORM-2]- liberated CO on attenuation of inflammatory responses in liver of an experimental animal model of thermal injury and to investigate the associated potential mechanisms. METHODS： Thirty-six mice were assigned to three groups in three respective experiments. In each experiment, mice in sham group （n = 4） received sham thermal injury, whereas mice in burn group （n = 4） received a 15% of total body surface area （TBSA） fullthickness thermal injury, and mice in burn ＋ CORM-2 group （n = 4） received the same thermal injury with immediate administration of CORM-2 （8 mg/kg, iv）. Hepatic tissue sections were stained with hematoxylin and eosin and examined under a light microscope. Levels of aminotransferases （ALT and AST） and nitric oxide （NO） were measured by biochemical methods. Tumor necrosis factor-α （TNF-α） and interleukin （IL-1β） activity, and the protein expression of iNOS and HO-1 in serum and tissue homogenates were assessed. In in vitro experiments, Kupffer cells were stimulated with LPS （10 μg/mL） for 4 h in the presence or absence of CORM-2 （10-100 μmol/L）. Subsequently, the expression levels of TNF-α and NO production were assessed. RESULTS： Pro-inflammatory mediators （TNF-α, IL- 1β, NO） in serum and liver homogenates of thermally injured mice were significantly reduced by CORM-2 administration. This was accompanied by a decrease in the expression of iNOS while an increase in the expression of HO-1 in the liver tissue. In parallel, the concentrations of TNF-α and NO in supernatants of LPS-stimulated Kupffer cells co-incubated with CORM-2 （10-100 μmol/L） were also markedly decreased.Histological examination demonstrated that CORM-2 could attenuate the leukocytes infiltration to the liver tissue. CONCLUSION： CORM-released CO modulates liver inflammation and significantly protects liver injury in burn mice by inhibiting the expression