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作 者:王伟[1] 蔡丽霞[1] 崔志瑞[1] 罗向阳[1]
机构地区:[1]郑州大学第三附属医院儿科,河南郑州450052
出 处:《中国妇幼保健》2014年第25期4162-4165,共4页Maternal and Child Health Care of China
基 金:河南省医学科技攻关计划项目〔201303092〕;河南省卫生科技创新型人才工程专项经费资助〔豫卫科201052〕
摘 要: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 effects of intrauterine inflammatory presensitization and hyperoxic exposure after birth on expressions of tumor suppressor protein (p53) and cell cycle regulatory factor (p21waf/eip[) gene in pneumonocytes of premature rats, explore their relationships with pathogenesis of new -type bronchopulmonary dysplasia (BPD) . Methods: The premature rats were randomly divided into normal saline + hyperoxia group, lipopolysaccharide (LPS) + hyperoxia group, LPS group and normal control group; RT - PCR was used to detect the expression levels of p53 and p21waf/cipl mRNA in pulmonary tissues of 8 rats randomly selected from each group on the first, the seventh and the fourteenth days after birth. Results: The expression level of p53 mRNA on the first day after birth in LPS group was statistically significantly higher than those in the other three groups ( P 〈 0.01 ), the expression level of p53 mRNA on the fourteenth day after birth in LPS + hyperoxia group was statistically significantly higher than those in the other three groups ( P 〈 0. 05 ) . The expression level of p21waf/cipl mRNA on the first day after birth in LPS group was statistically significantly higher than those in the other three groups (P 〈 0. 05 ) , the expression level of p21 waf/cipl mRNA on the fourteenth day after birth in LPS + hyperoxia group was statistically significantly higher than those in the other three groups (P 〈 0. 01 ) . Conclusion: Intrauterine inflammatory presensitization and hyperoxic exposure after birth may inhibit proliferation of pneumonocytes by p53 and p21 waf/cipl pathways, block the process of pulmonary alveoli, which may contribute to the occurrence of new - type BPD.
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