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目的:观察宫内炎性预敏和生后高氧暴露对肺细胞肿瘤抑制蛋白(p53)和肺细胞周期调节因子(p21waf/cip1)基因表达的影响,探讨其与新型支气管肺发育不良(BPD)发病机制之间的关系。方法:早产大鼠随机分为生理盐水+高氧组、LPS+高氧组、LPS组和正常对照组,于生后第1、7和14天随机取8只采用逆转录聚合酶链反应技术(RT-PCR)检测各组肺组织p53及p21waf/cip1mRNA的表达水平。结果:p53 mRNA表达LPS组在生后1天明显高于其他3组(P<0.01),LPS+高氧组在生后第14天明显高于其他3组(P<0.05)。p21waf/cip1mRNA的表达LPS组在生后第1天明显高于其它3组(P<0.05),LPS+高氧组在生后第14天明显高于其它3组(P<0.01)。结论:宫内炎性预敏及生后高氧暴露可能通过p53及p21waf/cip1途径抑制肺组织细胞增殖,使肺泡化进程受阻,进而可能导致新型BPD的发生。
OBJECTIVE: To observe the effect of intrauterine inflammatory pre-sensitivity and postnatal hyperoxia exposure on the expression of lung tumor suppressor protein (p53) and lung cell cycle regulators (p21waf / cip1) gene, and to explore its relationship with novel bronchopulmonary dysplasia (BPD) The relationship between pathogenesis. Methods: The premature rats were randomly divided into normal saline + hyperoxia group, LPS + hyperoxia group, LPS group and normal control group, and 8 rats were randomly selected on the 1st, 7th and 14th day after birth by reverse transcription polymerase chain reaction RT-PCR) was used to detect the expression of p53 and p21waf / cip1mRNA in lung tissues. Results: The expression of p53 mRNA in LPS group was significantly higher than that in the other three groups (P <0.01) on the 1st day after birth. LPS + hyperoxia group was significantly higher than the other three groups on the 14th day after birth (P <0.05). The expression of p21waf / cip1mRNA in LPS group was significantly higher than the other three groups on the first day after birth (P <0.05). The LPS + hyperoxia group was significantly higher than the other three groups on the 14th day after birth (P <0.01). CONCLUSION: Intrauterine inflammatory pre-sensitization and postnatal hyperoxia exposure may inhibit the proliferation of lung cells through the p53 and p21waf / cip1 pathways, obstructing the process of alveolar inflammation and possibly leading to the occurrence of new-type BPD.