中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2012年
2期
170-174
,共5页
黄一%闵家新%陈小波%吴秋平
黃一%閔傢新%陳小波%吳鞦平
황일%민가신%진소파%오추평
胸部损伤%肺泡%基因表达%细胞凋亡
胸部損傷%肺泡%基因錶達%細胞凋亡
흉부손상%폐포%기인표체%세포조망
Thoracic injuries%Pulmonary alveoli%Gene expression%Apoptosis
目的 探讨急性肺损伤(acute lung injury,ALI)后肺泡细胞的NIX基因及蛋白表达水平与创伤后肺泡细胞凋亡的关系及意义. 方法 建立大鼠严重胸部撞击伤模型,利用免疫组化、免疫印迹、RT-PCR等分子生物学技术分别检测创伤后6,12,24,48,72,96 h肺泡细胞NIX基因及其蛋白表达,通过Tunel试剂盒检测各时相点的肺泡细胞凋亡变化情况. 结果 (1)创伤组与对照组均存在NIX蛋白表达,NIX在伤后6h开始表达增高,并在48 h达到峰值,随后逐渐下降,96 h后接近致伤前水平.(2)除肺泡细胞外,NIX在血管内皮细胞及间质纤维细胞中也有较强表达；(3)伤后24 h肺泡细胞凋亡以支气管、血管内皮和肺泡上皮为主.伤后肺泡细胞凋亡率显著高于伤前水平(P＜0.01),于伤后72 h达到峰值,随后逐渐下降.(4)肺组织中NIX蛋白表达变化与肺泡细胞凋亡率变化呈显著性正相关(r=0.303,P＜0.01). 结论 NIX的上调参与了创伤后肺泡细胞凋亡的病理生理过程,其表达曲线与肺泡细胞凋亡率变化呈现一致性,这可能是创伤后肺泡细胞凋亡的分子学基础之一.
目的 探討急性肺損傷(acute lung injury,ALI)後肺泡細胞的NIX基因及蛋白錶達水平與創傷後肺泡細胞凋亡的關繫及意義. 方法 建立大鼠嚴重胸部撞擊傷模型,利用免疫組化、免疫印跡、RT-PCR等分子生物學技術分彆檢測創傷後6,12,24,48,72,96 h肺泡細胞NIX基因及其蛋白錶達,通過Tunel試劑盒檢測各時相點的肺泡細胞凋亡變化情況. 結果 (1)創傷組與對照組均存在NIX蛋白錶達,NIX在傷後6h開始錶達增高,併在48 h達到峰值,隨後逐漸下降,96 h後接近緻傷前水平.(2)除肺泡細胞外,NIX在血管內皮細胞及間質纖維細胞中也有較彊錶達；(3)傷後24 h肺泡細胞凋亡以支氣管、血管內皮和肺泡上皮為主.傷後肺泡細胞凋亡率顯著高于傷前水平(P＜0.01),于傷後72 h達到峰值,隨後逐漸下降.(4)肺組織中NIX蛋白錶達變化與肺泡細胞凋亡率變化呈顯著性正相關(r=0.303,P＜0.01). 結論 NIX的上調參與瞭創傷後肺泡細胞凋亡的病理生理過程,其錶達麯線與肺泡細胞凋亡率變化呈現一緻性,這可能是創傷後肺泡細胞凋亡的分子學基礎之一.
목적 탐토급성폐손상(acute lung injury,ALI)후폐포세포적NIX기인급단백표체수평여창상후폐포세포조망적관계급의의. 방법 건립대서엄중흉부당격상모형,이용면역조화、면역인적、RT-PCR등분자생물학기술분별검측창상후6,12,24,48,72,96 h폐포세포NIX기인급기단백표체,통과Tunel시제합검측각시상점적폐포세포조망변화정황. 결과 (1)창상조여대조조균존재NIX단백표체,NIX재상후6h개시표체증고,병재48 h체도봉치,수후축점하강,96 h후접근치상전수평.(2)제폐포세포외,NIX재혈관내피세포급간질섬유세포중야유교강표체；(3)상후24 h폐포세포조망이지기관、혈관내피화폐포상피위주.상후폐포세포조망솔현저고우상전수평(P＜0.01),우상후72 h체도봉치,수후축점하강.(4)폐조직중NIX단백표체변화여폐포세포조망솔변화정현저성정상관(r=0.303,P＜0.01). 결론 NIX적상조삼여료창상후폐포세포조망적병리생리과정,기표체곡선여폐포세포조망솔변화정현일치성,저가능시창상후폐포세포조망적분자학기출지일.
Objective To explore the relationship between the mRNA and protein expressions of NIX and the pulmonary alveolus apoptosis following severe acute lung injury (ALI). Methods Rat models of severe collision injury on the chest were built.The mRNA and protein expressions of NIX in the alveolar cells at 6,12,24,48,72 and 96 hours after injury were detected using immunohistochemistry,immunoblotting and RT-PCR.Meanwhile,apoptosis of the alveolar cells was checked at different time points with Tunel assay. Results The protein expression of NIX in the alveolar cells was observed both in experimental and control groups,which increased at 6 h post injury,peaked at 48 h and then declined till approaching the pre-injury level at 96 h.In the meantime,NIX showed a high expression both in the vascular endothelial cells (VECs) and the renal interstitial fibroblasts.The apoptosis of alveolar cells mainly presented in bronchi,blood vessel endothelium (BVE) and alveolar epithelium at 24 h post injury.The post-injury apoptosis rate of the alveolar cells was significantly higher than the pre-injury rate ( P ＜ 0.01 ),which reached the peak at 72 h and then decreased gradually.The changes of NIX protein in lung tissue showed a positive correlation with the apoptosis rate of alveolar cells after injury (r =0.303,P ＜ 0.01 ). Conclusions The up-regulated expression of NIX takes part in the pathophysiological process of apoptosis of the alveolar cells and shows consistency with the apoptosis rate change of the alveolar cells,as may be the molecular basis for apoptosis of the alveolar cells after ALI.
