国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2009年
6期
335-338,封3
,共5页
吴军%王良兴%应斌宇%狄枫%施孟如%郑易
吳軍%王良興%應斌宇%狄楓%施孟如%鄭易
오군%왕량흥%응빈우%적풍%시맹여%정역
肺动脉高压%双向凝胶电泳%基质辅助激光解析串联飞行时间质谱%野百合碱%钙网蛋白前体
肺動脈高壓%雙嚮凝膠電泳%基質輔助激光解析串聯飛行時間質譜%野百閤堿%鈣網蛋白前體
폐동맥고압%쌍향응효전영%기질보조격광해석천련비행시간질보%야백합감%개망단백전체
Pulmonary hypertension%Two-dimensional gel electrophoresis%MALDI-TOF-TOF-MS%Monocrotaline%Calreticulin precursor
目的 观察正常组与野百合碱致肺动脉高压组大鼠肺组织差异蛋白质组学的变化,在蛋白质组学水平探讨肺动脉高压形成机制.方法 雄性二级SD大鼠40只随机分为4组,每组10只,分别为正常对照组(N组)、溶剂对照组(C组)、野百合碱腹腔注射2周组(M2组)和野百合碱腹腔注射3周组(M3组).测定各组平均肺动脉压(mPAP)、平均颈动脉压(mCAP)、右心室质量比[RV/(LV+S)],制作光镜标本,测量肺血管重建指标肺细小动脉中膜厚度(PAMT),并进行统计学分析.对各组肺组织提取出的总蛋白质进行双向电泳,基质辅助激光解析串联飞行时间质谱鉴定蛋白质及NCBInr数据库检索.对鉴定的蛋白质进行分析.结果 N组与C组比较,mPAP、RV/(LV+S)、PAMT的差异均无统计学意义.N组、M2组、M3组的mPAP、RV/(LV+S)、PAMT均依次递增(P<0.05或P<0.01),表明肺动脉高压逐步形成.肺血管结构重建,右室肥大.肺动脉高压动物模型复制成功.通过双向凝胶电泳、基质辅助激光解析串联飞行时间质谱鉴定及数据库检索发现钙网蛋白前体在N组、C组表达几乎为0,在肺动脉高压组大量表达,可能在肺动脉高压形成、肺血管重建过程中发挥关键的作用.结论 钙网蛋白前体可能与肺动脉高压形成、肺血管重建密切相关,值得深入研究.
目的 觀察正常組與野百閤堿緻肺動脈高壓組大鼠肺組織差異蛋白質組學的變化,在蛋白質組學水平探討肺動脈高壓形成機製.方法 雄性二級SD大鼠40隻隨機分為4組,每組10隻,分彆為正常對照組(N組)、溶劑對照組(C組)、野百閤堿腹腔註射2週組(M2組)和野百閤堿腹腔註射3週組(M3組).測定各組平均肺動脈壓(mPAP)、平均頸動脈壓(mCAP)、右心室質量比[RV/(LV+S)],製作光鏡標本,測量肺血管重建指標肺細小動脈中膜厚度(PAMT),併進行統計學分析.對各組肺組織提取齣的總蛋白質進行雙嚮電泳,基質輔助激光解析串聯飛行時間質譜鑒定蛋白質及NCBInr數據庫檢索.對鑒定的蛋白質進行分析.結果 N組與C組比較,mPAP、RV/(LV+S)、PAMT的差異均無統計學意義.N組、M2組、M3組的mPAP、RV/(LV+S)、PAMT均依次遞增(P<0.05或P<0.01),錶明肺動脈高壓逐步形成.肺血管結構重建,右室肥大.肺動脈高壓動物模型複製成功.通過雙嚮凝膠電泳、基質輔助激光解析串聯飛行時間質譜鑒定及數據庫檢索髮現鈣網蛋白前體在N組、C組錶達幾乎為0,在肺動脈高壓組大量錶達,可能在肺動脈高壓形成、肺血管重建過程中髮揮關鍵的作用.結論 鈣網蛋白前體可能與肺動脈高壓形成、肺血管重建密切相關,值得深入研究.
목적 관찰정상조여야백합감치폐동맥고압조대서폐조직차이단백질조학적변화,재단백질조학수평탐토폐동맥고압형성궤제.방법 웅성이급SD대서40지수궤분위4조,매조10지,분별위정상대조조(N조)、용제대조조(C조)、야백합감복강주사2주조(M2조)화야백합감복강주사3주조(M3조).측정각조평균폐동맥압(mPAP)、평균경동맥압(mCAP)、우심실질량비[RV/(LV+S)],제작광경표본,측량폐혈관중건지표폐세소동맥중막후도(PAMT),병진행통계학분석.대각조폐조직제취출적총단백질진행쌍향전영,기질보조격광해석천련비행시간질보감정단백질급NCBInr수거고검색.대감정적단백질진행분석.결과 N조여C조비교,mPAP、RV/(LV+S)、PAMT적차이균무통계학의의.N조、M2조、M3조적mPAP、RV/(LV+S)、PAMT균의차체증(P<0.05혹P<0.01),표명폐동맥고압축보형성.폐혈관결구중건,우실비대.폐동맥고압동물모형복제성공.통과쌍향응효전영、기질보조격광해석천련비행시간질보감정급수거고검색발현개망단백전체재N조、C조표체궤호위0,재폐동맥고압조대량표체,가능재폐동맥고압형성、폐혈관중건과정중발휘관건적작용.결론 개망단백전체가능여폐동맥고압형성、폐혈관중건밀절상관,치득심입연구.
Objective To analyze systemically and unitarily the change proteins in the lung tissue when pulmonary hypertension forms through pulmonary tissue proteomic analysis between pulmonary hypertention rats induced by monocrotaline and normal rats. Methods Forty SD male rats were divided into four groups:normal group(group N), solvent control group(group C),2 week of monocrotaline(group M2), 3 week of monocrotaline (group M3). Mean pulmonary arterial pressure (mPAP), mean carotid arterial pressure(mCAP) ,weight ratio of right ventricle to left ventricle plus septum [ RV/(LV+ S)], thickness of pulmonary arterial media smooth cell layer(PAMT) were measured. Two-dimensional get eleetrophoresis of the total proteins from four groups, gel enzymolysis, MALDI-TOP-TOF-MS and retrieval databank in NCBInr were made. Results There were no significance in mPAP, RV/(LV+ S), PAMT of group N and group C. mPAP, RV/(LV+ S), PAMT of group N, group M2,group M3 rose up one by one( P <0.05 or P< 0. 01),which indicated that the pulmonary hypertention gradually formed, pneumoangiogram rebuilded, the right ventricle hypertrophy speared, and the rat model of pulmonary hypertention established successfully. The MALDI-TOF-TOF-MS discovered that there was hardly any expression of calreticulin precursor in group N and group C, and there was great expression in group M3. It could make great function in the development of pulmonary hypertension and pneumoangiogram rebuilding. Conclusions Calreticulin precursor could be related to the development of pulmonary hypertension and neumoangiogram rebuilding,it worths deep study.