胰岛素对大鼠急性肺损伤的肺血管内皮细胞核因子-kB和细胞间粘附分子-1表达的影响

目的 探讨胰岛素对急性肺损伤（ALI）大鼠肺血管内皮细胞核因子-kB（NF-kB）和细胞间粘附分子-1（ICAM-1）表达的影响。方法24只健康雄性SD大鼠（190-210g），随机分为正常对照组、ALI模型组、胰岛素干预组。观察肺组织病理形态，采用原位杂交技术半定量法和免疫组织化学染色检测肺血管内皮细胞的细胞间粘附分子-1（ICAM-1）mRNA和核因子-kB（NF-kB）蛋白的表达。结果（1）肺病理组织学结果显示胰岛素干预组肺病变局限且程度减轻；（2）ALI模型组肺血管内皮细胞ICAM-1mRNA表达（O．456±0．018）和NF-kB核染色阳性细胞百分比（0．542±0．009）与正常对照组（o．274土0．014，0．308±0．017）比较显著升高（均P〈0．05）；（3）胰岛素干预组ICAM-1mRNA表达（0．357±0．024）和NF-kB核染色阳性细胞百分比（0．427±0．018）比模型组明显减低（均P〈0．05），但与正常对照组比较仍较高（均P＜0．05）。结论ICAM-1和NF-kB在ALI显著增加，胰岛素可以抑制NF-kB和ICAM-1mRNA的表达，可能是其对抗ALI的作用机制之一。

INFLUENCE OF INSULIN ON THE EXPRESSIONS OF NF-kB AND ICAM-1mRNA IN PULMONARY VASCULAR ENDOTHELIAL CELLS OF ACUTE LUNG INJURY

Objective To investigate the effects of insulin on the acute lung injury （ALI） and the influence of insulin on expressions of NF-kB and ICAM-1mRNA in pulmonary vascular endothelial cells of ALl. Methods Twenty -four male Sprague-Dawley rats, 190-210g in body weight, were randomly divided into three experimental groups： a control group, a ALI model group and a insulin pretreatment group （n = 8, for each group ） . Lung specimens were examined by histopathological technique. Immunohistochemistry and in situ hybridization staining were used to semiquantitatively analyse the changes of NF-kB and ICAM-1mRNA expressions in pulmonary vascular endothelial cells. Result （1） The pathological changes in the insulin group were markedly milder than those in the ALl group. （2） In the ALI group, ICAM-1mRNA expression （0. 456±0. 018） and the percentage of positive cells of NF-kB nuclear staining （0. 542±0. 009） in pulmonary vascular endothelial cells were significantly higher than those in the control group （0. 274±0. 014, 0. 308±0. 017; P〈0.05 respectively） . （3） In the insulin group, ICAM-1mRNA expression （0. 357±0. 024） and the percentage of positive cells of NF-kB nuclear staining （0. 427±0. 018） in pulmonary vascular endothelial cells were significantly lower than those in the ALI group （0. 456±0. 018, 0. 542±0. 009; P〈0.05 respectively）, but higher than those in the control group （0. 274±0. 014, 0. 308±0. 017; P〈0.05 respectively） . Conclusion Insulin might significantly alleviate the degree of inflammatory injury by inhibiting the expressions of NF-kB and ICAM-1.