中华小儿外科杂志
中華小兒外科雜誌
중화소인외과잡지
CHINESE JOURNAL OF PEDIATRIC SURGERY
2008年
2期
118-121
,共4页
郭磊%赵玉岩%张世亮%朱世博%刘魁
郭磊%趙玉巖%張世亮%硃世博%劉魁
곽뢰%조옥암%장세량%주세박%류괴
畸形足,先天性%胰岛素样生长因子结合蛋白质6%维甲酸
畸形足,先天性%胰島素樣生長因子結閤蛋白質6%維甲痠
기형족,선천성%이도소양생장인자결합단백질6%유갑산
Congenital clubfoot%Insulin-like growth factor binding protein 6%Retinoin acid
目的 探讨大鼠先天性马蹄内翻足(CCF)软骨组织内胰岛素样生长因子结合蛋白6(IGFBP-6)的表达规律.方法 应用生物学活性物质全反式维甲酸(ATRA)构建大鼠CCF动物模型;光镜和透射电镜观测大鼠的足部软骨组织病理学改变;RT-PCR及Western印迹杂交检测胎鼠足部软骨组织中IGFBP-6 mRNA及蛋白质的表达水平.结果 120 mg/kg的ATRA诱导实验组35%的胎鼠出现CCF畸形,其他畸形包括:内翻足、小脑畸形、腭裂、无尾畸形等;在骨骼畸形胎鼠的足部距骨内软骨发生中心带缩小,软骨细胞数量减少,软骨细胞核内粗面内质网扩张,线粒体嵴紊乱;正常胎鼠软骨组织内IGFBP-6基因呈低水平表达状态,而骨骼畸形胎鼠IGFBP-6的mRNA和蛋白质表达则明显升高300%和197%(P＜0.05).结论 正常大鼠软骨组织内IGFBP-6基因有低表达.CCF大鼠软骨组织内IGFBP-6的高表达可能与骨骼发育畸形的发生密切相关.
目的 探討大鼠先天性馬蹄內翻足(CCF)軟骨組織內胰島素樣生長因子結閤蛋白6(IGFBP-6)的錶達規律.方法 應用生物學活性物質全反式維甲痠(ATRA)構建大鼠CCF動物模型;光鏡和透射電鏡觀測大鼠的足部軟骨組織病理學改變;RT-PCR及Western印跡雜交檢測胎鼠足部軟骨組織中IGFBP-6 mRNA及蛋白質的錶達水平.結果 120 mg/kg的ATRA誘導實驗組35%的胎鼠齣現CCF畸形,其他畸形包括:內翻足、小腦畸形、腭裂、無尾畸形等;在骨骼畸形胎鼠的足部距骨內軟骨髮生中心帶縮小,軟骨細胞數量減少,軟骨細胞覈內粗麵內質網擴張,線粒體嵴紊亂;正常胎鼠軟骨組織內IGFBP-6基因呈低水平錶達狀態,而骨骼畸形胎鼠IGFBP-6的mRNA和蛋白質錶達則明顯升高300%和197%(P＜0.05).結論 正常大鼠軟骨組織內IGFBP-6基因有低錶達.CCF大鼠軟骨組織內IGFBP-6的高錶達可能與骨骼髮育畸形的髮生密切相關.
목적 탐토대서선천성마제내번족(CCF)연골조직내이도소양생장인자결합단백6(IGFBP-6)적표체규률.방법 응용생물학활성물질전반식유갑산(ATRA)구건대서CCF동물모형;광경화투사전경관측대서적족부연골조직병이학개변;RT-PCR급Western인적잡교검측태서족부연골조직중IGFBP-6 mRNA급단백질적표체수평.결과 120 mg/kg적ATRA유도실험조35%적태서출현CCF기형,기타기형포괄:내번족、소뇌기형、악렬、무미기형등;재골격기형태서적족부거골내연골발생중심대축소,연골세포수량감소,연골세포핵내조면내질망확장,선립체척문란;정상태서연골조직내IGFBP-6기인정저수평표체상태,이골격기형태서IGFBP-6적mRNA화단백질표체칙명현승고300%화197%(P＜0.05).결론 정상대서연골조직내IGFBP-6기인유저표체.CCF대서연골조직내IGFBP-6적고표체가능여골격발육기형적발생밀절상관.
Objective To investigate the gene expression of insulin-like growth factor binding protein 6(IGFBP-6)in fetal rat with congenital talipes equinovarus(CCF).Methods The fetal rat models with CCF were constructed treated with all trans retinoic acid(ATRA)on pregnant day 10.The histopathologic characteristics of cartilaginous tissue in fetal foot with skeletal deformity was detected with light microscope and transmission electron microscope:The IGFBP-6 mRNA and protein level in cartilaginous tissue were detected by Reverse Transcription Polymerase Chain Reaction and Western Blotting.ResulIs ATRA(120mg/kg)induced single CCF or coalescent developmental skeleton defect in fetal rat(35%),such as cross-foot,cleft spine,cleft palate,rumpless and SO on.The chondrogenesis center of tarsal bones and quantity of chondrocyte were diminished.There were expanding rough endoplasmic reticulum,degradation of nuclear matrix,and disorder of mitochondria cristae in cell nucleus of chondrocyte.The expression of IGFBP-6 mRNA and protein were increased 300%and 197%in skeleton defect rat,compared with normal rat(P＜0.05).Conclusions There was low gene expression of IGFBP-6 in normal rat cartilaginous tissue and higher expression in CCF. The higher gene expression of IGFBP-6 may be induced the developmental skeleton defect in CCF rat.
