一氧化氮对急性肺损伤大鼠白细胞介素-6、环氧合酶-2的影响

Effect of nitric oxide on IL-6 and COX-2 in rats with acute lung injury

目的探讨吸入一氧化氮(NO)对急性肺损伤大鼠肺组织白细胞介素-6(IL-6)和环氧合酶-2(COX-2)的影响。方法脂多糖(LPS)气管内滴注,制造大鼠急性肺损伤模型,吸入NO,检测肺组织中IL-6和COX-2的表达。结果LPS气管内滴注后,肺组织中COX-2以及IL-6的含量较对照组(A组)明显增加,吸入20 mg/L的NO后,肺组织中IL-6降低;吸入100mg/L的NO时,肺组织中IL-6、COX-2含量明显升高。结论吸入20 mg/L的NO,可以减轻肺损伤的程度,而吸入100 mg/L的NO,则使肺组织的IL-6、COX-2含量增加,加重肺损伤的程度。

Objective To investigate the effect of inhaled nitric oxide （NO） on IL-6 and cox-2 in rat with acute lung injury （ALI） induced by lipopolysaccharide（LPS）. Methods Twenty -four Sprague-Dawley rats were randomly divided into four groups： group N, normal control group; group L, LPS instilled intratracheally to induce ALI; group Z1, LPS ＋ inhaled NO 20 mg/L and group Z2, LPS ＋ inhaled NO100 mg/L. Lung wet/dry weight ratios （W/D） were recorded to assess lung injury. The lung homogenates were prepared to detect IL-6 level by ELISA. The expression of COX-2 was detected by means of immunohistochemical staining. Results After LPS instilled, W/D ratio, IL-6 and COX-2 increased significantly. Compared with group L, W/D ratio decreased significantly in group Z1, but the ratio raised in group Z2 ; the level of IL-6 decreased sig- nificantly in group Z1; COX-2 level in group Z1 also decreased, but there was no statistical significant difference. Compared with group L, the level of IL-6 raised significantly in group Z2. Conclusion 20 mg/L NO inhalation decreased the level of IL-6 significantly, and the level of COX-2 also decreased. Low level of NO （20 mg/L） can down regulated inflammatory mediator expression in ALI rats. But high level NO （100 mg/L） might have deleterious effect on lung injury.