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目的近年研究发现急性肺损伤(ALI)是致新生儿肺出血的重要原因。大量研究表明肺表面活性蛋白A(SPA)和肿瘤坏死因子-α(TNFα)参与了ALI的损伤过程,但有关两者在肺出血新生儿支气管肺泡灌洗液(BALF)中的变化及关系鲜有报道。该研究旨在探讨SPA和TNFα在新生儿肺出血发生中的作用,两者间的关系及对预后的影响。方法采用斑点免疫印迹法和酶联免疫吸附法分别测定对照组(n=15),肺出血存活组急性期(n=14)、恢复期(n=14)和肺出血死亡组(n=6)新生儿BALF中SPA,TNFα和血清TNFα水平。结果存活组和死亡组新生儿肺出血急性期BALF中SPA含量(38.50±7.62,29.43±6.57)较对照组(44.88±7.48)显著降低(P=0.024,P=0),且死亡组SPA明显低于存活组急性期(P=0.015),存活组肺出血恢复期SPA水平(45.16±7.25)明显升高,接近对照组(P>0.05);而肺出血存活组和死亡组BALF中TNFα含量(208.54±64.69ng/L,319.16±46.79ng/L)较对照组(96.40±37.82ng/L)显著增加(P=0.011,P=0),死亡组比存活组急性期增加更明显(P=0),且BALF中TNFα的变化较血清中更明显,存活组恢复期BALF中TNFα水平(112.06±35.22ng/L)明显下降,接近对照组(P>0.05);肺出血患儿BALF中SPA水平的下降与TNFα的增高呈负相关(r=0.635,P=0.003)。结论SPA和TNFα参与了新生儿肺出血的肺损伤过程,为从SPA及细胞因子角度进一步认识新生儿肺出血的发病机制提供了实验依据,为新生儿肺出血的早期防治及预后判断提供了一种新的方法。
In recent years, studies have found that acute lung injury (ALI) is an important cause of neonatal pulmonary hemorrhage. A large number of studies have shown that pulmonary surfactant protein A (SPA) and tumor necrosis factor-α (TNFα) are involved in the process of ALI injury, but their relationship with bronchoalveolar lavage fluid (BALF) There are reports. The purpose of this study was to investigate the role of SPA and TNFα in the development of neonatal pulmonary hemorrhage, the relationship between the two and prognosis. Methods Immunohistochemistry and enzyme-linked immunosorbent assay were used to detect the apoptosis in the control group (n = 15), the pulmonary hemorrhage survival group (n = 14), the recovery phase (n = ) SPA, TNFα and serum TNFα levels in neonates with BALF. Results The SPA of BALF in survivors and death patients was significantly lower (P = 0.024, P = 0) than that of the control group (38.50 ± 7.62,29.43 ± 6.57) in the acute stage of neonatal pulmonary hemorrhage (P = 0.024, P = 0) (P = 0.015). The level of SPA in COPD survivors (45.16 ± 7.25) was significantly higher than that in control group (P> 0.05). The level of TNFα in BALF of survivors and death patients (P = 0.011, P = 0) in the control group (208.54 ± 64.69ng / L, 319.16 ± 46.79ng / L) was significantly higher than that in the control group (96.40 ± 37.82ng / L) = 0), and the change of TNFα in BALF was more obvious than that in serum. The level of TNFα in BALF of 112.36 ± 35.22ng / L BALF in surviving group was significantly lower than that in control group (P> 0.05) The decrease of SPA level was negatively correlated with the increase of TNFα (r = 0.635, P = 0.003). Conclusion SPA and TNFα are involved in the process of lung injury induced by neonatal pulmonary hemorrhage and provide an experimental basis for further understanding the pathogenesis of neonatal pulmonary hemorrhage from the perspective of SPA and cytokines and provide a basis for the early prevention and prognosis of neonatal pulmonary hemorrhage A new way.