中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
46期
7452-7457
,共6页
蒋玉权%刘继春%叶晓健%胡跃%瞿金涛
蔣玉權%劉繼春%葉曉健%鬍躍%瞿金濤
장옥권%류계춘%협효건%호약%구금도
组织构建%组织工程%黄韧带%腰椎%碱性成纤维细胞因子%转化生长因子β1%结缔组织生长因子%胶原蛋白
組織構建%組織工程%黃韌帶%腰椎%堿性成纖維細胞因子%轉化生長因子β1%結締組織生長因子%膠原蛋白
조직구건%조직공정%황인대%요추%감성성섬유세포인자%전화생장인자β1%결체조직생장인자%효원단백
ligamentum flavum%spinal stenosis%transforming growth factor beta1%fibroblast growth factor 2%connective tissue growth factor
背景:腰椎黄韧带肥厚是临床上引起腰椎管狭窄的主要因素之一,但其分子机制仍不是非常清楚。目的:分析纤维化相关细胞因子碱性成纤维细胞生长因子、转化生长因子β1和结缔组织生长因子在腰椎黄韧带肥厚过程中的作用。方法:取临床手术所取黄韧带,对照组6例(椎管内占位且无腰椎不稳患者黄韧带)、突出组(单纯腰椎间盘突出症患者黄韧带)6例、腰椎管狭窄症组6例。采用实时定量RT-PCR的方法检测各组黄韧带中碱性成纤维细胞生长因子、转化生长因子β1、结缔组织生长因子及Ⅰ、Ⅲ、Ⅴ型胶原蛋白的mRNA含量,分析3个细胞因子在黄韧带肥厚过程中的作用。结果与结论:腰椎管狭窄症组碱性成纤维细胞生长因子mRNA表达均明显高于突出组和对照组(均P <0.05);腰椎管狭窄症组转化生长因子β1mRNA在3组中的表达明显高于对照组和突出组(均P <0.01);结缔组织生长因子 mRNA 3组间差异无显著性意义(P >0.05)。腰椎管狭窄症组Ⅰ型胶原蛋白mRNA表达明显高于突出组和对照组(均P <0.05);Ⅲ型胶原蛋白、Ⅴ型胶原蛋白mRNA表达3组之间差异无显著性意义(P >0.05)。结果说明碱性成纤维细胞生长因子、转化生长因子β1在腰椎黄韧带肥厚形成过程中有重要作用,引起黄韧带肥厚的主要胶原产物为Ⅰ型胶原蛋白。
揹景:腰椎黃韌帶肥厚是臨床上引起腰椎管狹窄的主要因素之一,但其分子機製仍不是非常清楚。目的:分析纖維化相關細胞因子堿性成纖維細胞生長因子、轉化生長因子β1和結締組織生長因子在腰椎黃韌帶肥厚過程中的作用。方法:取臨床手術所取黃韌帶,對照組6例(椎管內佔位且無腰椎不穩患者黃韌帶)、突齣組(單純腰椎間盤突齣癥患者黃韌帶)6例、腰椎管狹窄癥組6例。採用實時定量RT-PCR的方法檢測各組黃韌帶中堿性成纖維細胞生長因子、轉化生長因子β1、結締組織生長因子及Ⅰ、Ⅲ、Ⅴ型膠原蛋白的mRNA含量,分析3箇細胞因子在黃韌帶肥厚過程中的作用。結果與結論:腰椎管狹窄癥組堿性成纖維細胞生長因子mRNA錶達均明顯高于突齣組和對照組(均P <0.05);腰椎管狹窄癥組轉化生長因子β1mRNA在3組中的錶達明顯高于對照組和突齣組(均P <0.01);結締組織生長因子 mRNA 3組間差異無顯著性意義(P >0.05)。腰椎管狹窄癥組Ⅰ型膠原蛋白mRNA錶達明顯高于突齣組和對照組(均P <0.05);Ⅲ型膠原蛋白、Ⅴ型膠原蛋白mRNA錶達3組之間差異無顯著性意義(P >0.05)。結果說明堿性成纖維細胞生長因子、轉化生長因子β1在腰椎黃韌帶肥厚形成過程中有重要作用,引起黃韌帶肥厚的主要膠原產物為Ⅰ型膠原蛋白。
배경:요추황인대비후시림상상인기요추관협착적주요인소지일,단기분자궤제잉불시비상청초。목적:분석섬유화상관세포인자감성성섬유세포생장인자、전화생장인자β1화결체조직생장인자재요추황인대비후과정중적작용。방법:취림상수술소취황인대,대조조6례(추관내점위차무요추불은환자황인대)、돌출조(단순요추간반돌출증환자황인대)6례、요추관협착증조6례。채용실시정량RT-PCR적방법검측각조황인대중감성성섬유세포생장인자、전화생장인자β1、결체조직생장인자급Ⅰ、Ⅲ、Ⅴ형효원단백적mRNA함량,분석3개세포인자재황인대비후과정중적작용。결과여결론:요추관협착증조감성성섬유세포생장인자mRNA표체균명현고우돌출조화대조조(균P <0.05);요추관협착증조전화생장인자β1mRNA재3조중적표체명현고우대조조화돌출조(균P <0.01);결체조직생장인자 mRNA 3조간차이무현저성의의(P >0.05)。요추관협착증조Ⅰ형효원단백mRNA표체명현고우돌출조화대조조(균P <0.05);Ⅲ형효원단백、Ⅴ형효원단백mRNA표체3조지간차이무현저성의의(P >0.05)。결과설명감성성섬유세포생장인자、전화생장인자β1재요추황인대비후형성과정중유중요작용,인기황인대비후적주요효원산물위Ⅰ형효원단백。
BACKGROUND:Ligamentum flavum hypertrophy is one of the most important factors of lumbar spinal stenosis, but the molecular mechanism is stil not very clear. OBJECTIVE:To explore the role of basic fibroblast growth factor, connective tissue growth factor and transforming growth factor β1 in hypertrophy of the lumbar ligamentum flavum. METHODS: The ligamentum flavum samples were divided into three groups according to different diseases: control group (acquired from the patients with lumbar spinal canal tumor,n=6), lumbar disc herniation (LDH) group (acquired from the patients with LDH,n=6) and lumbar spinal stenosis (LSS) group (acquired from the patients with LSS,n=6). Then the mRNA expressions of basic fibroblast growth factor, connective tissue growth factor, transforming growth factor β1 and colagen I, III, V of the ligamentum flavum were detected using real-time quantitative RT-PCR method. The roles of basic fibroblast growth factor, connective tissue growth factor and transforming growth factor β1 were explored. RESULTS AND CONCLUSION:The expression of basic fibroblast growth factor mRNA in the LSS group was significantly higher than that in the LDH and control groups (bothP < 0.05); the expression of connective tissue growth factor mRNA was not found statisticaly different among the three groups, although it was slightly higher in the LSS group (P> 0.05); the expression of transforming growth factor β1 mRNA was significantly higher in the LSS group than in the LDH and control groups (bothP < 0.01). The colagen I mRNA expressed significantly higher in the LSS group than the LDH and control groups (bothP < 0.05), but both the colagen III and V mRNA showed no significant difference among the three groups (P> 0.05). This study indicate that both basic fibroblast growth factor and transforming growth factor β1 play important roles in the formation process of the lumbar ligamentum flavum hypertrophy, and the main type of the colagen in the hypertrophied ligamentum flavum is colagen I.