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作 者:张婷[1] 卢红艳[1] 王秋霞[1] 高楚楚[1]
出 处:《基础医学与临床》2013年第11期1460-1464,共5页Basic and Clinical Medicine
基 金:江苏省自然科学基金(BK2011485);镇江市社会发展项目(SH2011022)
摘 要:目的探讨内质网应激(ERS)相关蛋白GRP78和caspase-12在支气管肺发育不良(BPD)大鼠肺组织中的表达及意义。方法利用早产新生大鼠持续高氧暴露复制BPD模型。将48只SD早产鼠随机分为高氧组和空气组。高氧组持续暴露于85%O2中,空气组置于同一室内常压空气中。两组分别于建模后7、14和21 d取肺组织,HE染色观察肺组织病理改变并行辐射状肺泡计数(RAC),TUNEL法检测细胞凋亡,实时荧光定量RT-PCR和Western blot技术分别检测GRP78和caspase-12 mRNA和蛋白表达。结果高氧组早产大鼠出现肺结构简单化,肺泡变大及数量减少等类似BPD病理学特征。与同日龄空气组相比,高氧组RAC明显减少,细胞凋亡明显增加,GRP78和caspase-12 mRNA和蛋白表达均明显升高(P<0.01),且随高氧暴露时间延长,呈逐渐上升趋势。结论 GRP78和caspase-12表达增加可能与BPD发生发展有关。Objective To investigate the expression of endoplasmie reticulum stress-related protein GRP78 and easpase-12 in the lung of bronehopulmonary dysplasis (BPD) rats. Methods Hyperoxia-induced preterm rat mod- el of BPD was established. Forty-eight premature Sprague-Dawley rats were randomly divided into hyperoxia group and air group. The hyperoxia group was continually exposed to hyperoxia (85 % ) while the air group in room air. Lung tissues were obtained at 7, 14 and 21 days after exposing to either room atmosphere or hyperoxia. The chan- ges of pulmonary histopathology were observed by hematoxylin-eosin (HE) staining and radical alveolar count (RAC). Apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL). The expressions of GRP78, caspase-12 mRNA and protein were detected by real-time quantitative RT-PCR and western blot respectively. Re- sults The lung of hyperoxia premature rats showed simple alveolar structure, fewer and larger alveoli, which shares morphologic similarities to BPD. Compared with the air group, hyperoxia exposure resulted in lower RAC and significant apoptosis. In addition, the expression levels of GRP78 and caspase-12 mRNA and protein increasedsignificantly (P 〈 0. 01 ) and had a up-regulated trend. Conclusions The increased expression of GRP78 and caspase-12 may be involved in the pathogenesis of BPD.
关 键 词:GRP78 CASPASE-12 高浓度氧 支气管肺发育不良
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