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
8期
1430-1434
,共5页
朱红%曹文%李娅娟%杨选影%夏长所
硃紅%曹文%李婭娟%楊選影%夏長所
주홍%조문%리아연%양선영%하장소
生物材料%材料生物相容性%组织工程复合支架材料%6-磷酸果糖%转化生长因子 β1%Ⅰ型胶原%肌腱粘连%兔%省级基金%生物材料图片文章
生物材料%材料生物相容性%組織工程複閤支架材料%6-燐痠果糖%轉化生長因子 β1%Ⅰ型膠原%肌腱粘連%兔%省級基金%生物材料圖片文章
생물재료%재료생물상용성%조직공정복합지가재료%6-린산과당%전화생장인자 β1%Ⅰ형효원%기건점련%토%성급기금%생물재료도편문장
背景:有实验证实外源性6-磷酸果糖能降低肌腱细胞Ⅰ型胶原的产生量,减轻肌腱术后粘连的形成.目的:观察6-磷酸果糖对肌腱术后粘连形成的影响.方法:取72只兔行中趾屈指肌腱切断吻合,随机分成实验组与对照组(n=36),分别于腱鞘内注入6-磷酸果糖与生理盐水,术后4,8周后行肌腱粘连检测、生物力学测定、组织学观察和扫描电镜观察;术后1,2,4,8周采用原位杂交方法测定肌腱转化生长因子β1和Ⅰ型胶原 mRNA 的表达.结果与结论:术后4,8周,与对照组比较,实验组肌腱缝合处光滑,屈趾肌腱滑动距离较长,肌腱滑动受限较轻(P <0.05),但两组最大抗断裂载荷差异无显著性意义(P >0.05);扫描电镜和组织学观察结果显示,对照组胶原纤维排列紊乱,实验组胶原纤维排列整齐.实验组转化生长因子β1和Ⅰ型胶原mRNA 表达水平均低于对照组(P <0.05).证实6-磷酸果糖能有效抑制转化生长因子β1在肌腱损伤修复中的作用,减轻粘连形成.
揹景:有實驗證實外源性6-燐痠果糖能降低肌腱細胞Ⅰ型膠原的產生量,減輕肌腱術後粘連的形成.目的:觀察6-燐痠果糖對肌腱術後粘連形成的影響.方法:取72隻兔行中趾屈指肌腱切斷吻閤,隨機分成實驗組與對照組(n=36),分彆于腱鞘內註入6-燐痠果糖與生理鹽水,術後4,8週後行肌腱粘連檢測、生物力學測定、組織學觀察和掃描電鏡觀察;術後1,2,4,8週採用原位雜交方法測定肌腱轉化生長因子β1和Ⅰ型膠原 mRNA 的錶達.結果與結論:術後4,8週,與對照組比較,實驗組肌腱縫閤處光滑,屈趾肌腱滑動距離較長,肌腱滑動受限較輕(P <0.05),但兩組最大抗斷裂載荷差異無顯著性意義(P >0.05);掃描電鏡和組織學觀察結果顯示,對照組膠原纖維排列紊亂,實驗組膠原纖維排列整齊.實驗組轉化生長因子β1和Ⅰ型膠原mRNA 錶達水平均低于對照組(P <0.05).證實6-燐痠果糖能有效抑製轉化生長因子β1在肌腱損傷脩複中的作用,減輕粘連形成.
배경:유실험증실외원성6-린산과당능강저기건세포Ⅰ형효원적산생량,감경기건술후점련적형성.목적:관찰6-린산과당대기건술후점련형성적영향.방법:취72지토행중지굴지기건절단문합,수궤분성실험조여대조조(n=36),분별우건초내주입6-린산과당여생리염수,술후4,8주후행기건점련검측、생물역학측정、조직학관찰화소묘전경관찰;술후1,2,4,8주채용원위잡교방법측정기건전화생장인자β1화Ⅰ형효원 mRNA 적표체.결과여결론:술후4,8주,여대조조비교,실험조기건봉합처광활,굴지기건활동거리교장,기건활동수한교경(P <0.05),단량조최대항단렬재하차이무현저성의의(P >0.05);소묘전경화조직학관찰결과현시,대조조효원섬유배렬문란,실험조효원섬유배렬정제.실험조전화생장인자β1화Ⅰ형효원mRNA 표체수평균저우대조조(P <0.05).증실6-린산과당능유효억제전화생장인자β1재기건손상수복중적작용,감경점련형성.
@@@@BACKGROUND: It has been confirmed that exogenous mannose-6-phosphate can inhibit type Ⅰcol agen production in tendon cells and prevent tendon adhesion after repair of flexor tendon injury. OBJECTIVE: To investigate the preventive effect of mannose-6-phosphate on adhesion formation fol owing flexor tendon repair.METHODS: Seventy-two adult New Zealand White rabbit forepaws underwent sharp transection of the middle digit flexor digitorum profundus and immediate repair, and then were randomly divided into experimental (injected with mannose-6-phosphate) and control (injected with normal saline) groups. Tendons were harvested at 4 and 8 weeks postoperatively, and biomechanics testing, histological evaluation and scanning electron microscope observation were conducted. In situ hybridization method was performed to determine the mRNA expression of transforming growth factor beta 1 and type Ⅰcol agen. RESULTS AND CONCLUSION: At 4 and 8 weeks after operation, the suture line was smooth, the gliding excursion ratio of the flexor tendon was higher, and the tendon sliding was constrained less in the experimental group as compared with the control group (P < 0.05). However, there was no significant difference in the tensile strength of tendon anastomosis between the two groups (P > 0.05). Scanning electron microscope and histological observation showed that col agen fibers arranged irregularly in the control group, but arranged regularly in the experimental group. The in situ hybridization examination revealed that transforming growth factor beta 1 and type Ⅰ col agen mRNA expression in the experimental group was lower than that in the control group (P < 0.05). These findings indicate that mannose-6-phosphate can inhibit the function of the transforming growth factor beta 1 effectively in the flexor tendon repair and prevent adhesion formation.