论文部分内容阅读
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-κB(NF-κB)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-κB(NF-κB)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(0.456±0.018)和NF-κB核染色阳性细胞百分比(0.542±0.009)与正常对照组(0.274±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-κB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-κB在ALI显著增加,胰岛素可以抑制NF-κB和ICAM-1mRNA的表达,可能是其对抗ALI的作用机制之一。
Objective To investigate the effect of insulin on the expression of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in pulmonary vascular endothelial cells of acute lung injury (ALI) rats. Methods Twenty-four healthy male SD rats (190-210g) were randomly divided into normal control group, ALI model group and insulin intervention group. The pathological changes of lung tissue were observed. The ICAM-1 mRNA and NF-κB protein in pulmonary vascular endothelial cells were detected by semi-quantitative in situ hybridization and immunohistochemical staining expression. Results (1) The results of histopathology showed that the lung lesions in the insulin intervention group were limited and lessened. (2) The expression of ICAM-1mRNA in pulmonary vascular endothelial cells (0.456 ± 0.018) and the percentage of nuclear NF-κB positive cells (P <0.05). (3) The expression of ICAM-1mRNA in the insulin intervention group (0.357 ± 0.024) and NF-κB nuclear staining positive cells were significantly higher than those in the normal control group (0.274 ± 0.014,0.308 ± 0.017) (0.427 ± 0.018) was significantly lower than that of the model group (all P <0.05), but still higher than that of the normal control group (all P <0.05). Conclusions ICAM-1 and NF-κB are significantly increased in ALI. Insulin can inhibit the expression of NF-κB and ICAM-1 mRNA, which may be one of its mechanisms of action against ALI.