基质金属蛋白酶和胶原在创伤后关节软骨组织中的表达及其意义
发布时间：2018-10-17 22:12
【摘要】： 目的 采用手术方法建立大鼠膝关节骨软骨缺损及表面软骨缺损动物模型,通过检测胶原表达变化探讨不同关节软骨缺损自我修复的能力,通过检测基质金属蛋白酶(matrix metalloproteinase,MMP)在损后伤关节软骨组织中的表达变化,探讨损伤导致关节软骨退变的病理学机制。 方法 取雌性SD大鼠48只,随机分成A、B、C三组,A组18只,在双膝关节股骨髌面制作骨软骨缺损直径3.0mm,深度3.0mm,以缺损底部出现渗血为宜;B组18只,在双膝关节股骨髁间制作表面软骨缺损宽度0.3mm,深度0.3mm,缺损底部无渗血,不穿透软骨下骨板;C组12只,双膝关节只做关节囊切开,不做任何处置直接缝合,为假手术对照组。分别于术后4、8、12W三个时间点取材,实验组每个时间点处死6只大鼠,对照组每个时间点处死4只大鼠。取双膝关节原切口,充分显露股骨远端关节面,于股骨髁上垂直于骨干截下股骨远端。将标本放置于固定脱钙后制作石蜡切片,行HE、甲苯胺兰染色、Ⅰ型胶原、Ⅱ型胶原、MMP-2、MMP-3、MMP-9免疫组化染色。 结果 A组术后4W缺损中有少量新生组织生成,8W及12W可见到纤维组织填充,三个时间点修复组织细胞外基质Ⅰ型胶原免疫组化染色阳性,Ⅱ型胶原免疫组化染色阴性,关节软骨组织中MMP-2、MMP-3、MMP-9表达增高(与C组比较有显著性差异,P＜0.05)。B组表面软骨缺损4W及8W未见修复迹象,12W可见微量纤维组织填充,其细胞外基质Ⅰ型胶原免疫组化染色阳性,Ⅱ型胶原免疫组化染色阴性,B组关节软骨组织术后三个时间点MMP-2、MMP-3、MMP-9表达均增高(与C组比较有显著性差异,P＜0.05)。C组三个时间点均为正常关节软骨组织,Ⅰ型胶原免疫组化染色阴性,Ⅱ型胶原免疫组化染色阳性,MMP-2、MMP-3、MMP-9低度表达,无形态学异常改变。 结论 大鼠骨软骨缺损在间充质细胞的参与下以纤维形式进行自我修复,修复组织无法恢复正常关节面的平整,是非透明软骨组织。表面关节软骨缺损由于未穿透软骨下骨板,无间充质细胞参与,很难实现自我修复,随着时间推移缺损周围的软骨变薄,出现不同程度的退变。通过手术方法可以在大鼠膝关节建立合理的骨软骨缺损及表面软骨缺损动物模型,并可以用来考察移植方法修复软骨缺损的疗效。机械性损伤可以导致关节软骨细胞外基质成分发生改变,丧失其原有的生物学特性而退变,基质降解素(MMP-3)和明胶酶(MMP-2、9)在损伤后的软骨组织中表达增高,使细胞外基质的降解增加,是导致关节软骨退变的重要因素。
[Abstract]:Objective to establish an animal model of osteochondral defect and surface cartilage defect of knee joint in rats by surgical method, and to explore the ability of self-repair of different articular cartilage defects by detecting the changes of collagen expression. By detecting the expression of matrix metalloproteinase (matrix metalloproteinase,MMP) in articular cartilage after injury, the pathological mechanism of articular cartilage degeneration caused by injury was investigated. Methods Forty eight female SD rats were randomly divided into three groups: group A (n = 18), group B (n = 18). The surface cartilage defects were made in the femoral condyle of both knee joints with a width of 0.3 mm and a depth of 0.3 mm. There was no bleeding at the bottom of the defect and no penetration of the subchondral bone plate, while in group C, 12 knees were treated with joint capsule incision without any disposal and direct suture, which was used as the sham operation control group. 6 rats were killed at each time point in the experimental group and 4 rats in the control group were killed at each time point. The joint surface of the distal femur was fully exposed through the original incision of the knee joint, and was perpendicular to the shaft of the femoral condyle to amputate the distal femur. The specimens were fixed and decalcified to make paraffin sections. The specimens were stained with HE, toluidine blue, type 鈪，
本文编号：2278176
[Abstract]:Objective to establish an animal model of osteochondral defect and surface cartilage defect of knee joint in rats by surgical method, and to explore the ability of self-repair of different articular cartilage defects by detecting the changes of collagen expression. By detecting the expression of matrix metalloproteinase (matrix metalloproteinase,MMP) in articular cartilage after injury, the pathological mechanism of articular cartilage degeneration caused by injury was investigated. Methods Forty eight female SD rats were randomly divided into three groups: group A (n = 18), group B (n = 18). The surface cartilage defects were made in the femoral condyle of both knee joints with a width of 0.3 mm and a depth of 0.3 mm. There was no bleeding at the bottom of the defect and no penetration of the subchondral bone plate, while in group C, 12 knees were treated with joint capsule incision without any disposal and direct suture, which was used as the sham operation control group. 6 rats were killed at each time point in the experimental group and 4 rats in the control group were killed at each time point. The joint surface of the distal femur was fully exposed through the original incision of the knee joint, and was perpendicular to the shaft of the femoral condyle to amputate the distal femur. The specimens were fixed and decalcified to make paraffin sections. The specimens were stained with HE, toluidine blue, type 鈪，
本文编号：2278176
本文链接：https://www.wllwen.com/yixuelunwen/shiyanyixue/2278176.html
最近更新
教材专著
