摘要
背景:基质细胞衍生因子1/CXC趋化因子受体4信号通路在骨关节炎的发病中起关键作用。目的:探讨AMD3100体外阻断基质细胞衍生因子1/CXC趋化因子受体4信号通路后对培养的关节软骨组织Ⅱ型胶原、聚集蛋白聚糖mRNA表达及Ⅱ型胶原蛋白表达的影响。方法:将骨关节炎软骨和创伤性截肢患者正常软骨分别分为3个小组即实验组,实验对照组,空白对照组。将其置于含基质细胞衍生因子1和AMD3100,含基质细胞衍生因子1和MAB310,只含基质细胞衍生因子1的培养液培养。结果与结论:实验组软骨组织内的Ⅱ型胶原和聚集蛋白聚糖mRNA表达量、Ⅱ型胶原蛋白含量高于实验对照组和空白对照组(P<0.05)。可见基质细胞衍生因子1通过基质细胞衍生因子1/CXC趋化因子受体4信号通路诱导人关节软骨中Ⅱ型胶原和聚集蛋白聚糖的降解;AMD3100可阻断该信号通路及减少软骨中Ⅱ型胶原和聚集蛋白聚糖的降解,延缓关节软骨组织的退变;AMD3100不能使已退变的骨关节炎软骨内的Ⅱ型胶原和聚集蛋白聚糖含量恢复到正常水平。
BACKGROUND：Stromal cell derived factor-1（SDF-1）/chemokine receptor 4（CXCR4） signal pathway plays a key role in the pathogenesis of osteoarthritis.OBJECTIVE：To explore the effect of SDF-1/CXCR4 signal pathway on the expression of type Ⅱ collagen and aggrecan mRNA of the synthesis in human articular cartilage after blocking the SDF-1/CXCR4 signal pathway with AMD3100.METHODS：The cartilage blocks from osteoarthritis patients who had total knee replacement and normal cartilage blocks from patients who had traumatic amputation were collected and divided into three groups：experimental group,experimental control group and blank control group.The three groups were cultured in the nutrient solution containing of SDF-1 and AMD3100,SDF-1 and MAB310,as well as SDF-1 only,respectively.RESULTS AND CONCLUSION：The expressions of type Ⅱ collagen and aggrecan mRNA,as well as type Ⅱ collagen content in the experimental group was higher than those in the experimental control group and blank control group（P0.05）.These results suggest that SDF-1 can induce the degradation of type Ⅱ collagen and aggrecan thruogh the SDF-1/CXCR4 signaling pathway.Besides,AMD3100 can block SDF-1/CXCR4 signal pathway and reduce the degradation of type II collagen and aggrecan,and therefore slow down the degeneration of articular cartilage.But AMD3100 cannot recover type II collagen and aggrecan in osteoarthritis cartilage to normal levels
出处
《中国组织工程研究》
CAS
CSCD
2012年第46期8607-8610,共4页
Chinese Journal of Tissue Engineering Research
基金
国家自然科学基金资助项目(30860286)~~
