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目的:观察宫内炎性暴露对胎鼠及早产大鼠肺细胞凋亡及肺Bax和Bcl-2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:定期受孕的Sprague Dawley(SD)大鼠随机分为脂多糖(LPS)组和生理盐水组(对照组),于孕15天羊膜腔内注射LPS/无菌生理盐水。两组动物均于胚胎19天(E19)及出生后第1、3、5、7天(P1、P3、P5、P7)各随机取8只,应用脱氧核糖核酸转移酶介导的细胞凋亡标记技术(TUNEL)原位检测细胞凋亡及逆转录-聚合酶链反应技术(RT-PCR)检测各组肺组织Bax和Bcl-2 mRNA表达水平。结果:LPS组随鼠龄递增,肺细胞凋亡数目逐渐增加,至P3达高峰,P5后逐渐下降;在E19~P7均高于对照组,且在E19、P1及P3与对照组相比差异有统计学意义(P<0.05);LPS组Bax mRNA的表达在E19~P7均高于对照组,且在E19~P5与对照组相比差异有统计学意义(P<0.05);Bcl-2 mRNA的表达LPS组在E19~P7均较对照组低,且在E19~P5与对照组相比差异有统计学意义(P<0.05)。结论:宫内炎性暴露可能通过调控Bax/Bcl-2的表达使肺组织细胞过度凋亡,进而导致新型BPD的发生。
Objective: To observe the effects of intrauterine inflammatory exposure on the apoptosis of lung cells and the expression of Bax and Bcl-2 genes in fetal rats and premature rats, and to explore its relationship with the pathogenesis of new-type bronchopulmonary dysplasia (BPD). Methods: Sprague Dawley rats were randomly divided into LPS group and normal saline group (control group). LPS / sterile saline was injected into the amniotic cavity 15 days after their pregnancy. Eight animals were randomly selected from each of the two groups at embryonic day 19 (E19) and on days 1, 3, 5 and 7 (P1, P3, P5 and P7). DNA- Apoptosis was detected by TUNEL in situ and the expression of Bax and Bcl-2 mRNA in lung tissues of each group were detected by reverse transcription-polymerase chain reaction (RT-PCR). Results: The number of apoptotic lung cells in LPS group increased gradually with the increase of age, reached the peak of P3 and decreased gradually after P5, but higher in E19 ~ P7 than that in control group (P <0.05). The expression of Bax mRNA in LPS group was higher than that in control group at E19 ~ P7, and there was significant difference between E19 ~ P5 and control group (P <0.05); Bcl-2 The expression of mRNA in LPS group was lower than that in control group at E19 ~ P7, and there was significant difference between E19 ~ P5 and control group (P <0.05). Conclusion: Intrauterine inflammatory exposure may induce excessive apoptosis of lung cells by regulating the expression of Bax / Bcl-2, leading to the occurrence of new type of BPD.