Carbon liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice

瞄准：为了决定碳(公司) 是否解放了从，共同释放分子在热地受伤的老鼠的小肠稀释白血球渗入。方法：36 只老鼠被分到四个组。在假冒的组的老鼠(n = 9 ) 经历了到假冒的热损害；在灼伤组的老鼠(n = 9 ) 收到了 15% 全部的身体表面区域完整厚度的热损害；在灼伤 + CORM-2 的老鼠组织(n = 9 ) 与 tricarbonyldichlororuthenium (II ) 的立即的管理经历了到一样的热损害更暗淡的 CORM-2 (8 mg/kg， i.v ) ；并且在 burn+DMSO 的老鼠组织(n = 9 ) 与 0.5% DMSO/saline 的 160 muL 大丸药注射的立即的管理经历了到一样的热损害。小肠的组织学的改变和粒细胞渗入被估计。Polymorphonuclear neutrophil (PMN ) 累积(myeloperoxidase 试金) 在老鼠被估计中间回肠。-kappaB, 表示细胞间的粘附 molecule-1 (ICAM-1 ) 铺平的原子因素(NF ) 的激活并且可诱导他我氧合酶在中间回肠被估计。结果：有 CORM-2 的热地受伤的老鼠的处理稀释了 PMN 累积并且在小肠阻止了 NF-kappaB 的激活。这被减少在 ICAM-1 的表示伴随。在平行、导致灼伤的粒细胞渗入在中间回肠显著地在与 CORM-2 对待的灼伤老鼠被减少。结论：释放球茎的公司由防碍 NF-kappaB 激活和 ICAM-1 的蛋白质表示，因此压制 endothelial 的支持粘合剂的显型在热地受伤的鼠标的小肠稀释白血球渗入。

AIM： To determine whether Carbon （CO） liberated from CO-releasing molecules attenuates leukocyte infiltration in the small intestine of thermally injured mice. METHODS： Thirty-six mice were assigned to four groups. Mice in the sham group （n = 9） were underwent to sham thermal injury; mice in the burn group （n = 9） received 15% total body surface area full-thickness thermal injury; mice in the burn ＋ CORM-2 group （n = 9） were underwent to the same thermal injury with immediate administration of tricarbonyldichlororut henium （11） dimer CORM-2 （8 mg/kg, i.v.）; and mice in the burn＋DMSO group （n = 9） were underwent to the same thermal injury with immediate administration of 160 IJL bolus injection of 0.5% DMSO/saline. Histological alterations and granulocyte infiltration of the small intestine were assessed. Polymorphonuclear neutrophil （PMN） accumulation （myeloperoxidase assay） was assessed in mice mid-ileum. Activation of nuclear factor （NF）-KB, expression levels of intercellular adhesion molecule-1 （ICAM-1） and inducible heme oxygenase in mid-ileum were assessed. RESULTS： Treatment of thermally injured mice with CORM-2 attenuated PMN accumulation and prevented activation of NF-kB in the small intestine. This was accompanied by a decrease in the expression of ICAM-1. In parallel, burn-induced granulocyte infiltration in mid- ileum was markedly decreased in the burn mice treated with CORM-2. CONCLUSION： CORM-released CO attenuates leukocyteinfiltration in the small intestine of thermally injured mice by interfering with NF-KB activation and protein expression of ICAM-1, and therefore suppressing the pro-adhesive phenotype of endothelial cells.