临床儿科杂志
臨床兒科雜誌
림상인과잡지
2013年
10期
959-963
,共5页
内质网应激%细胞凋亡%支气管肺发育不良%大鼠
內質網應激%細胞凋亡%支氣管肺髮育不良%大鼠
내질망응격%세포조망%지기관폐발육불량%대서
endoplasmic reticulum stress%apoptosis%bronchopulmonary dysplasia%rat
目的：通过检测内质网应激（ERS）相关因子葡萄糖调节蛋白（GRP78）及C/EBP同源蛋白（CHOP）在支气管肺发育不良（BPD）大鼠肺组织中的表达及其与肺泡上皮细胞凋亡的关系，探讨ERS介导肺泡上皮细胞凋亡在BPD发病机制中的作用。方法将24只新生SD大鼠随机分为对照组和BPD组，每组12只。BPD组大鼠暴露于85%高氧中，对照组大鼠置于空气中。在实验7、14和21天每组各处死4只大鼠，通过免疫组化检测GRP78在肺组织中的表达和分布，实时定量PCR（real-time PCR）和免疫印迹（Western blot）技术检测GRP78及CHOP的表达变化，原位末端标记（TUNEL）法检测肺组织细胞凋亡。结果在各时间点，BPD组肺组织的细胞凋亡数，GRP78、CHOP mRNA及蛋白表达与对照组相比，差异有统计学意义（P均<0.01）。随时间延长，BPD组肺组织的细胞凋亡数，GRP78、CHOP mRNA及蛋白表达水平呈上升趋势，差异有统计学意义（P均<0.01）。结论高氧可启动ERS并可能通过激活CHOP通路介导肺泡上皮细胞凋亡，参与BPD的发病过程。
目的：通過檢測內質網應激（ERS）相關因子葡萄糖調節蛋白（GRP78）及C/EBP同源蛋白（CHOP）在支氣管肺髮育不良（BPD）大鼠肺組織中的錶達及其與肺泡上皮細胞凋亡的關繫，探討ERS介導肺泡上皮細胞凋亡在BPD髮病機製中的作用。方法將24隻新生SD大鼠隨機分為對照組和BPD組，每組12隻。BPD組大鼠暴露于85%高氧中，對照組大鼠置于空氣中。在實驗7、14和21天每組各處死4隻大鼠，通過免疫組化檢測GRP78在肺組織中的錶達和分佈，實時定量PCR（real-time PCR）和免疫印跡（Western blot）技術檢測GRP78及CHOP的錶達變化，原位末耑標記（TUNEL）法檢測肺組織細胞凋亡。結果在各時間點，BPD組肺組織的細胞凋亡數，GRP78、CHOP mRNA及蛋白錶達與對照組相比，差異有統計學意義（P均<0.01）。隨時間延長，BPD組肺組織的細胞凋亡數，GRP78、CHOP mRNA及蛋白錶達水平呈上升趨勢，差異有統計學意義（P均<0.01）。結論高氧可啟動ERS併可能通過激活CHOP通路介導肺泡上皮細胞凋亡，參與BPD的髮病過程。
목적：통과검측내질망응격（ERS）상관인자포도당조절단백（GRP78）급C/EBP동원단백（CHOP）재지기관폐발육불량（BPD）대서폐조직중적표체급기여폐포상피세포조망적관계，탐토ERS개도폐포상피세포조망재BPD발병궤제중적작용。방법장24지신생SD대서수궤분위대조조화BPD조，매조12지。BPD조대서폭로우85%고양중，대조조대서치우공기중。재실험7、14화21천매조각처사4지대서，통과면역조화검측GRP78재폐조직중적표체화분포，실시정량PCR（real-time PCR）화면역인적（Western blot）기술검측GRP78급CHOP적표체변화，원위말단표기（TUNEL）법검측폐조직세포조망。결과재각시간점，BPD조폐조직적세포조망수，GRP78、CHOP mRNA급단백표체여대조조상비，차이유통계학의의（P균<0.01）。수시간연장，BPD조폐조직적세포조망수，GRP78、CHOP mRNA급단백표체수평정상승추세，차이유통계학의의（P균<0.01）。결론고양가계동ERS병가능통과격활CHOP통로개도폐포상피세포조망，삼여BPD적발병과정。
Objectives To investigate the expressions of endoplasmic reticulum stress (ERS)-related factors, glucose regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), in lungs of rats with bronchopulmonary dysplasia (BPD) and their relationship with pneumonocyte apoptosis, and further to explore the role of ERS-induced apoptosis in the pathogen-esis of BPD. Methods A total of 24 neonatal SD rats were randomly divided into control group and BPD group with 12 rats each. Rats in BPD group were exposed to 85%O2, while rats in the control group were exposed to air. Four rats in each group were sacriifced at 7, 14 and 21 days respectively after exposure. The expression of GRP78 in the lung tissues was examined by immunohistochemistry, the mRNA and protein levels of GRP78 and CHOP were detected respectively by real-time PCR and Western blot, and the apoptosis in lung cells were evaluated by TdT-mediated dUTP nick end labeling (TUNEL) assay. Results The mRNA and protein levels of GRP78 and CHOP, and the cell apoptosis in BPD group were signiifcantly different from those in control group (P<0.01) at different time points and increased over the time of hyperoxic exposure (P<0.01). Conclusions En-doplasmic reticulum stress may be initiated by hyperoxic exposure and apoptosis is induced via CHOP signal pathway, which is involved in the pathogenesis of BPD.
