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目的探讨肺表面活性物质蛋白B(SP-B)参与新生儿呼吸窘迫综合征(RDS)发病的可能机制。方法选择无血缘关系的60例因RDS死亡的新生儿为RDS组,其中≤31周亚组、32～36周亚组及≥37周亚组每组各纳入20例;选择无血缘关系的60例因其他疾病死亡的新生儿为对照组,胎龄与RDS组以1:1相匹配。所有研究对象均在死后30min内取肺组织,采用免疫印迹方法分析SP-B蛋白在肺部的表达,实时定量-聚合酶链反应(RT-PCR)方法分析肺部SP-B信使RNA(mRNA)表达。SP-BmRNA和SP-B蛋白缺陷的频率采用统计学分析。结果 RDS组8例肺组织SP-B蛋白表达减少或缺失,其中6例完全缺失;对照组1例肺组织SP-B蛋白表达减少;此9例均分布在≥37周亚组。RDS组SP-BmRNA相对表达量显著低于对照组[(2.55±1.90)比(3.74±1.12),t=4.145,P<0.001];≤31周亚组RDS组与对照组差异无统计学意义[(2.35±1.34)比(2.66±1.14),t=0.776,P>0.05];32～36周亚组和≥37周亚组中,RDS组均低于对照组[32～36周亚组:(2.23±1.22)比(3.80±0.25),t=5.661,P<0.001;≥37周亚组:(3.08±2.74)比(4.75±0.49),t=2.682,P<0.05]。SP-B蛋白和mRNA水平成同向表达减少。结论转录和翻译水平均介入了SP-B蛋白的最后表达,SP-BmRNA和SP-B蛋白减少参与了RDS发病。
Objective To investigate the possible mechanism of pulmonary surfactant protein B (SP-B) involved in the pathogenesis of neonatal respiratory distress syndrome (RDS). Methods Sixty unrelated newborns died of RDS were selected as RDS group. Among them, ≤31 weeks subgroup, 32-36 weeks subgroup and ≥37 weeks subgroup were enrolled in each of 20 cases; Cases of neonatal death due to other diseases as a control group, gestational age and RDS group 1: 1 match. All of the subjects took the lung tissue within 30 min after death, the expression of SP-B protein in the lungs was analyzed by immunoblotting, and the SP-B messenger RNA in lungs was analyzed by real-time quantitative polymerase chain reaction (RT-PCR) mRNA) expression. The frequency of SP-B mRNA and SP-B protein defects was statistically analyzed. Results In the RDS group, the expression of SP-B protein in 8 cases of lung tissue was decreased or disappeared, of which 6 cases were completely deleted. The expression of SP-B protein in the lung tissue of 1 case was decreased in the control group. All 9 cases were distributed in the group of ≥37 weeks. The relative expression level of SP-B mRNA in RDS group was significantly lower than that in control group [(2.55 ± 1.90) vs (3.74 ± 1.12), t = 4.145, P <0.001]. There was no significant difference between RDS group and control group [(2.35 ± 1.34) vs (2.66 ± 1.14), t = 0.776, P> 0.05]. In the 32-36 weeks subgroup and the ≧ 37 weeks subgroup, the RDS group was lower than the control group [32-36 weeks subgroup : (2.23 ± 1.22) vs (3.80 ± 0.25), t = 5.661, P <0.001; ≥37 weeks subgroup: (3.08 ± 2.74) vs (4.75 ± 0.49), t = 2.682, P <0.05]. The expression of SP-B protein and mRNA decreased in the same direction. Conclusion Both transcriptional and translational levels involve the final expression of SP-B protein, and the decrease of SP-B mRNA and SP-B protein is involved in the pathogenesis of RDS.