中国组织工程研究与临床康复
中國組織工程研究與臨床康複
중국조직공정연구여림상강복
JOURNAL OF CLINICAL REHABILITATIVE TISSUE ENGINEERING RESEARCH
2010年
7期
1204-1207
,共4页
股骨头坏死%血管内皮生长因子%反转录聚合酶链式反应%动物实验%中国白兔%组织工程
股骨頭壞死%血管內皮生長因子%反轉錄聚閤酶鏈式反應%動物實驗%中國白兔%組織工程
고골두배사%혈관내피생장인자%반전록취합매련식반응%동물실험%중국백토%조직공정
背景:动物实验显示,激素可导致股骨头内毛细血管明显充盈不良,单位面积内毛细血管密度明显下降,软骨下松质骨内微血管数明显减少,但具体机制尚不清楚.目的:观察激素诱导骨坏死过程中血管内皮生长因子的表达变化.方法:将中国大耳白兔以抽签法随机分马血清加甲基强的松龙组与单纯甲基强的松龙组.参考Matsui的方法制备典型的兔骨坏死动物模型,马血清加甲基强的松龙组经耳缘静脉注射马血清10 mL/kg,间隔2周后,再次相同剂量及方法注射马血清,间隔2周后腹腔注射甲基强的松龙45 mg/(kg·d),连续5 d.对照组腹腔注射甲基强的松龙45 mg/(kg·d),连续5 d.采用RT-RCR技术检测两组用药前、用药后7,14 d,第1次用激素后1,3,7,21,35,49 d骨组织中血管内皮生长因子基因表达,并进行微血管计数.结果与结论:使用马血清后7 d血管内皮生长因子明显增高,此后呈缓慢回落状态,在应用激素后1 d回落到正常用药前水平,随着应用激素时间的延长,血管内皮生长因子mRNA的表达量逐渐减低,以第7,21天为显著(P<0.05),以后逐渐回升,但不能达到正常水平;微血管计数数量逐渐减少,在21 d时减少最明显,与血管内皮生长因子表达量呈正相关.结果提示糖皮质激素抑制了骨组织中血管内皮生长因子的表达,从而抑制了骨内新生血管的形成,使骨组织局部缺血、缺氧状态难以修复重建:血管内皮生长因子的表达与骨组织微血管数量及骨坏死程度密切相关.
揹景:動物實驗顯示,激素可導緻股骨頭內毛細血管明顯充盈不良,單位麵積內毛細血管密度明顯下降,軟骨下鬆質骨內微血管數明顯減少,但具體機製尚不清楚.目的:觀察激素誘導骨壞死過程中血管內皮生長因子的錶達變化.方法:將中國大耳白兔以抽籤法隨機分馬血清加甲基彊的鬆龍組與單純甲基彊的鬆龍組.參攷Matsui的方法製備典型的兔骨壞死動物模型,馬血清加甲基彊的鬆龍組經耳緣靜脈註射馬血清10 mL/kg,間隔2週後,再次相同劑量及方法註射馬血清,間隔2週後腹腔註射甲基彊的鬆龍45 mg/(kg·d),連續5 d.對照組腹腔註射甲基彊的鬆龍45 mg/(kg·d),連續5 d.採用RT-RCR技術檢測兩組用藥前、用藥後7,14 d,第1次用激素後1,3,7,21,35,49 d骨組織中血管內皮生長因子基因錶達,併進行微血管計數.結果與結論:使用馬血清後7 d血管內皮生長因子明顯增高,此後呈緩慢迴落狀態,在應用激素後1 d迴落到正常用藥前水平,隨著應用激素時間的延長,血管內皮生長因子mRNA的錶達量逐漸減低,以第7,21天為顯著(P<0.05),以後逐漸迴升,但不能達到正常水平;微血管計數數量逐漸減少,在21 d時減少最明顯,與血管內皮生長因子錶達量呈正相關.結果提示糖皮質激素抑製瞭骨組織中血管內皮生長因子的錶達,從而抑製瞭骨內新生血管的形成,使骨組織跼部缺血、缺氧狀態難以脩複重建:血管內皮生長因子的錶達與骨組織微血管數量及骨壞死程度密切相關.
배경:동물실험현시,격소가도치고골두내모세혈관명현충영불량,단위면적내모세혈관밀도명현하강,연골하송질골내미혈관수명현감소,단구체궤제상불청초.목적:관찰격소유도골배사과정중혈관내피생장인자적표체변화.방법:장중국대이백토이추첨법수궤분마혈청가갑기강적송룡조여단순갑기강적송룡조.삼고Matsui적방법제비전형적토골배사동물모형,마혈청가갑기강적송룡조경이연정맥주사마혈청10 mL/kg,간격2주후,재차상동제량급방법주사마혈청,간격2주후복강주사갑기강적송룡45 mg/(kg·d),련속5 d.대조조복강주사갑기강적송룡45 mg/(kg·d),련속5 d.채용RT-RCR기술검측량조용약전、용약후7,14 d,제1차용격소후1,3,7,21,35,49 d골조직중혈관내피생장인자기인표체,병진행미혈관계수.결과여결론:사용마혈청후7 d혈관내피생장인자명현증고,차후정완만회락상태,재응용격소후1 d회락도정상용약전수평,수착응용격소시간적연장,혈관내피생장인자mRNA적표체량축점감저,이제7,21천위현저(P<0.05),이후축점회승,단불능체도정상수평;미혈관계수수량축점감소,재21 d시감소최명현,여혈관내피생장인자표체량정정상관.결과제시당피질격소억제료골조직중혈관내피생장인자적표체,종이억제료골내신생혈관적형성,사골조직국부결혈、결양상태난이수복중건:혈관내피생장인자적표체여골조직미혈관수량급골배사정도밀절상관.
BACKGROUND: Animal experiments show that hormone can induce femoral capillaries poor filling, decrease capillaries density in unit area, and reduce capillaries in cancellous bone inferior to cartilage. However, the involved mechanism remains unclear.OBJECTIVE: To explore the changes of vascular endothelial growth factor (VEGF) during the progress of glucocorticoid induced osteonecrosis.METHODS: The Chinese white rabbits were randomly divided into horse serum plus prednisone group and pradnisone alone group. Typical osteonecrosis model was established by Matsui Method. 10 mL/kg horse serum was injected into horse serum plusprednisone group through the ear margin veins, followed by additional injection after 2 weeks and intraparit0neal injection of prednisone, 45 mg/kg per day for 5 consecutive days. The control group was only subjected to prednisona, 45 mg/kg per day for 5 consecutive days. The VEGF expression was observed by means of reverse transcription polymerase chain react.ion (RT-PCR)before, 7, 14 days after administration, 1, 3, 7, 21, 35 and 49 days following the first application of hormone. The capillaries were quantified.RESULTS ANDCONCLUSION: The VEGF was significantly increased 7 days following horse serum, and gradually decreased to levels before treatment 1 days following hormone. The VEGF mRNA, expression decreased with increasing hormone treatment, in particular at 7 and 21 days (P < 0.05), but cannot restore to normal level. Micrevascular count was decreased gradually, and at 21 days decreased to the minimum, positively correlated with VEGF expression. Results show that adrenal glucocorticoid inhibited VEGF expression in bone tissue and restrained angiogenesis, resulting in ischemia and hypoxia of the local environment in bone tissue. VEGF expression highly correlates with microvascular count and osteonecrosis degree.