论文部分内容阅读
目的观察宫内炎性暴露对胎鼠及早产大鼠肺细胞凋亡的影响,探讨其与新型支气管肺发育不良发病机制之间的关系。方法定期受孕的Sprague Daw ley(SD)大鼠随机分为脂多糖(lipopolysaccharide,LPS)组(LPS组)和生理盐水组(对照组),两组动物均于胚胎19 d(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。结果LPS组肺细胞凋亡在E19~P3均较对照组高,且与对照组相比,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/Bc l-2的表达途径使肺组织细胞过度凋亡,进而导致BPD的发生。
Objective To observe the effect of intrauterine inflammatory exposure on the apoptosis of lung cells in fetal rats and premature rats, and to explore its relationship with the pathogenesis of new bronchopulmonary dysplasia. Methods Sprague Dawley rats were randomly divided into LPS group (LPS group) and normal saline group (control group). Both groups were on embryonic day 19 (E19) and after birth On the 1st, 3rd, 5th and 7th day (P1, P3, P5, P7), 8 mice were randomly selected, and apoptosis was detected by TUNEL in situ. Results The apoptosis of lung cells in LPS group was higher than that in control group from E19 to P3, and the difference was statistically significant (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 BPD.