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目的:研究油酸(OA)致大鼠急性肺损伤(ALI)时,P-选择素(Ps)、细胞间粘附分子-1(ICAM-1)和核因子-κB(NFκ-B)在肺组织中的表达及褪黑素(MT)对肺组织的保护作用及其机制。方法:将48只SD大鼠随机分为4组(n=12),对照组(Control)、油酸组(OA)、MT+OA组,SB203580+OA组。采用尾静脉注射油酸的方法建立大鼠ALI的模型,测定肺系数,光镜下观察大鼠肺组织形态学改变,并通过免疫组织化学染色技术观察肺组织中Ps、ICAM-1和NFκ-B的表达变化。结果:与control组相比,OA组大鼠肺系数明显升高(P<0.05);肺组织损伤严重,肺泡间隔明显增宽,肺泡腔及肺间质弥漫性炎细胞浸润;Ps、ICAM-1和NFκ-B的阳性表达信号明显增强(P<0.05);应用MT和SB203580均显著缓解上述变化(P<0.05)。结论:MT对ALI时的肺组织起明显的保护作用,其保护机制可能与抑制Ps、ICAM-1和NFκ-B的表达有关。
Objective: To investigate the effects of oleic acid (OA) on the expression of P-selectin (Ps), intercellular adhesion molecule-1 (ICAM-1) and nuclear factor-κB (NFκB) in acute lung injury (ALI) Lung tissue and the protective effect of melatonin (MT) on lung tissue and its mechanism. Methods: Forty eight Sprague Dawley rats were randomly divided into 4 groups (n = 12), control group, oleic acid group (OA), MT + OA group and SB203580 + OA group. The rat model of ALI was established by injecting oleic acid into the caudal vein. The lung coefficient was determined. The morphological changes of the lung tissue were observed under light microscope. The expressions of Ps, ICAM-1 and NFκ-2 in lung tissues were observed by immunohistochemical staining. B expression changes. Results: Compared with the control group, the lung coefficient of OA group was significantly increased (P <0.05); the lung tissue was damaged severely, the alveolar septum was obviously broadened, the infiltration of diffuse inflammatory cells in the alveolar space and interstitium was found; Ps, ICAM- 1 and NFκ-B were significantly increased (P <0.05). Both MT and SB203580 significantly alleviated the above changes (P <0.05). CONCLUSION: MT can obviously protect the lung tissue from ALI. The protective mechanism may be related to the inhibition of the expression of Ps, ICAM-1 and NFκ-B.