中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
11期
1965-1971
,共7页
孙虹%张明辉%翁立新%孙同柱
孫虹%張明輝%翁立新%孫同柱
손홍%장명휘%옹립신%손동주
组织构建%组织构建与生物活性因子%酸性成纤维细胞生长因子%受体%细胞外调节蛋白激酶%缺血-再灌注损伤%小肠%小肠绒毛上皮细胞%其他基金%组织构建图片文章
組織構建%組織構建與生物活性因子%痠性成纖維細胞生長因子%受體%細胞外調節蛋白激酶%缺血-再灌註損傷%小腸%小腸絨毛上皮細胞%其他基金%組織構建圖片文章
조직구건%조직구건여생물활성인자%산성성섬유세포생장인자%수체%세포외조절단백격매%결혈-재관주손상%소장%소장융모상피세포%기타기금%조직구건도편문장
背景:细胞外调节蛋白激酶和酸性成纤维细胞生长因子受体2在肠缺血-再灌注损伤修复中的作用尚无研究报道.目的:观察大鼠肠缺血-再灌注损伤后外源性酸性成纤维细胞生长因子对细胞外调节蛋白激酶和酸性成纤维细胞生长因子受体2表达的影响,探讨细胞外调节蛋白激酶和酸性成纤维细胞生长因子受体2与酸性成纤维细胞生长因子促进创伤修复的关系.方法:以大鼠肠系膜上动脉夹闭45 min 造成肠缺血-再灌注损伤模型,于再灌注即刻应用酸性成纤维细胞生长因子行干预.分别于再灌注2,6,12,24 h 取大鼠小肠组织标本,利用免疫组化和 RT-PCR 检测酸性成纤维细胞生长因子受体的表达及免疫组化检测细胞外调节蛋白激酶表达的规律.结果与结论:在正常大鼠,酸性成纤维细胞生长因子受体2主要分布在小肠绒毛上皮细胞的肠腔侧、侧壁和小肠隐窝朝向隐窝腔的一侧细胞膜上.缺血-再灌注初期,酸性成纤维细胞生长因子受体2及细胞外调节蛋白激酶的表达未发生明显变化,但随着再灌注时间的延长表达水平逐渐提高,并于再灌注后6-12 h 达高峰.经酸性成纤维细胞生长因子治疗后,大鼠小肠组织小肠黏膜损伤程度减轻,酸性成纤维细胞生长因子受体2及细胞外调节蛋白激酶的表达量高于未治疗大鼠.结果表明缺血-再灌注损伤后,酸性成纤维细胞生长因子干预可上调酸性成纤维细胞生长因子受体2及细胞外调节蛋白激酶的表达,提示外源性酸性成纤维细胞生长因子通过促进内源性酸性成纤维细胞生长因子受体2和细胞外调节蛋白激酶的生成可能是其参与内脏损伤修复的机制之一.
揹景:細胞外調節蛋白激酶和痠性成纖維細胞生長因子受體2在腸缺血-再灌註損傷脩複中的作用尚無研究報道.目的:觀察大鼠腸缺血-再灌註損傷後外源性痠性成纖維細胞生長因子對細胞外調節蛋白激酶和痠性成纖維細胞生長因子受體2錶達的影響,探討細胞外調節蛋白激酶和痠性成纖維細胞生長因子受體2與痠性成纖維細胞生長因子促進創傷脩複的關繫.方法:以大鼠腸繫膜上動脈夾閉45 min 造成腸缺血-再灌註損傷模型,于再灌註即刻應用痠性成纖維細胞生長因子行榦預.分彆于再灌註2,6,12,24 h 取大鼠小腸組織標本,利用免疫組化和 RT-PCR 檢測痠性成纖維細胞生長因子受體的錶達及免疫組化檢測細胞外調節蛋白激酶錶達的規律.結果與結論:在正常大鼠,痠性成纖維細胞生長因子受體2主要分佈在小腸絨毛上皮細胞的腸腔側、側壁和小腸隱窩朝嚮隱窩腔的一側細胞膜上.缺血-再灌註初期,痠性成纖維細胞生長因子受體2及細胞外調節蛋白激酶的錶達未髮生明顯變化,但隨著再灌註時間的延長錶達水平逐漸提高,併于再灌註後6-12 h 達高峰.經痠性成纖維細胞生長因子治療後,大鼠小腸組織小腸黏膜損傷程度減輕,痠性成纖維細胞生長因子受體2及細胞外調節蛋白激酶的錶達量高于未治療大鼠.結果錶明缺血-再灌註損傷後,痠性成纖維細胞生長因子榦預可上調痠性成纖維細胞生長因子受體2及細胞外調節蛋白激酶的錶達,提示外源性痠性成纖維細胞生長因子通過促進內源性痠性成纖維細胞生長因子受體2和細胞外調節蛋白激酶的生成可能是其參與內髒損傷脩複的機製之一.
배경:세포외조절단백격매화산성성섬유세포생장인자수체2재장결혈-재관주손상수복중적작용상무연구보도.목적:관찰대서장결혈-재관주손상후외원성산성성섬유세포생장인자대세포외조절단백격매화산성성섬유세포생장인자수체2표체적영향,탐토세포외조절단백격매화산성성섬유세포생장인자수체2여산성성섬유세포생장인자촉진창상수복적관계.방법:이대서장계막상동맥협폐45 min 조성장결혈-재관주손상모형,우재관주즉각응용산성성섬유세포생장인자행간예.분별우재관주2,6,12,24 h 취대서소장조직표본,이용면역조화화 RT-PCR 검측산성성섬유세포생장인자수체적표체급면역조화검측세포외조절단백격매표체적규률.결과여결론:재정상대서,산성성섬유세포생장인자수체2주요분포재소장융모상피세포적장강측、측벽화소장은와조향은와강적일측세포막상.결혈-재관주초기,산성성섬유세포생장인자수체2급세포외조절단백격매적표체미발생명현변화,단수착재관주시간적연장표체수평축점제고,병우재관주후6-12 h 체고봉.경산성성섬유세포생장인자치료후,대서소장조직소장점막손상정도감경,산성성섬유세포생장인자수체2급세포외조절단백격매적표체량고우미치료대서.결과표명결혈-재관주손상후,산성성섬유세포생장인자간예가상조산성성섬유세포생장인자수체2급세포외조절단백격매적표체,제시외원성산성성섬유세포생장인자통과촉진내원성산성성섬유세포생장인자수체2화세포외조절단백격매적생성가능시기삼여내장손상수복적궤제지일.
BACKGROUND: Role of extracel ular signal-regulated kinase and acidic fibroblast growth factor receptor 2 in intestinal ischemia-reperfusion injury repair has not been reported. OBJECTIVE: To identify the changes in extracel ular signal-regulated kinase and acidic fibroblast growth factor receptor 2 regulated by exogenous acidic fibroblast growth factor (acidic fibroblast growth factor) fol owing intestinal ischemia-reperfusion injury in rats, and to explore the role of extracel ular signal-regulated kinase and acidic fibroblast growth factor receptor 2 in acidic fibroblast growth factor-induced injury repair. METHODS: Intestinal ischemia-reperfusion injury models were produced in rats by clamping the superior mesenteric artery for 45 minutes, and then acidic fibroblast growth factor administration was applied immediately after modeling. Tissue specimens were col ected at 2, 6, 12, and 24 hours after reperfusion. The expressions of acidic fibroblast growth factor receptor 2 and extracel ular signal-regulated kinase were detected by immunohistochemistry and reverse transcription-PCR. RESULTS AND CONCLUSION: The expressions of acidic fibroblast growth factor receptor 2 and extracel ular signal-regulated kinase increased gradual y after ischemia-reperfusion injury and peaked at 6-12 hours after reperfusion. Acidic fibroblast growth factor administration relieved intestinal mucosa injury and increased the expressions of acidic fibroblast growth factor receptor 2 and extracel ular signal-regulated kinase. These results suggest that acidic fibroblast growth factor administration can upregulate the expressions of acidic fibroblast growth factor receptor 2 and extracel ular signal-regulated kinase after ischemia-reperfusion injury, indicating exogenous acidic fibroblast growth factor can participate in visceral damage repair via the activation of endogenous acidic fibroblast growth factor receptor 2 and extracel ular signal-regulated kinase.