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目的 观察Krüppel样因子-5(KLF-5)和基质金属蛋白酶-9(MMP-9)表达活性与人膝关节软骨血管及神经纤维侵入之间的关系.方法 从 20例行全膝关节置换术的患者中,选取切除的31个关节标本;将每个标本切割成2～3块,并分成磨损组(n=29)和无磨损组(n=17).结果 在磨损组的关节软骨潮线附近有血管化发生,扫描电镜也证实血管结构的存在;关节软骨的神经侵袭仅发生于血管化的标本;与无磨损的关节软骨区比较,磨损区的血管化和神经支配数量明显增加(P<0.05).在磨损组的关节软骨中,KLF-5、MMP-9的表达活性明显高于无磨损组(P<0.05),而且与血管侵袭程度正相关.结论 增加的KLF-5和MMP-9表达可能是导致骨关节炎软骨退变和血管化的重要机制之一.Abstract： Objective To investigate the relationship between the expression neurovascular invasion in osteophytes in osteoarthritis (OA). Methods Thirty-one articular cartilage samples were collected from 20 patients who had undergone total knee arthroplasty (TKA), and each sample was divided into two groups: no change (NC,n=17) and severe change (SC,n=29) according to Mankin score and safranin O staining. Neurovascular markers protein gene product (PGP) 9.5 and CD34, and the expression of KLF-5, MMP-9 were detected by using immunohistochemistry. Results Vascular channels were observed in both NC and SC sections. In SC sections, 16/29 (55.2%) sections displayed vessels entering the calcified cartilage, which was more than that in NC group (2/17, 11.8%,P<0.05). The frequency of neurovascular invasion was significantly different between SC and NC (P<0.05). Innervation always accompanied vascular invasion at the osteochondral junction. The severity of neurovascular invasion was positively correlated with the expression of KLF-5 and MMP-9 in chondrocytes at the same site that was significantly different between SC and NC. Conclusion KLF-5-induced MMP-9 expression may be involved in cartilage matrix degradation and vascularization. 相似文献
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目的 研究苯磺酸氨氯地平(AM)、阿托伐他汀(AT)单独及联合用药对球囊损伤诱导的血管新生内膜形成影响及机制.方法 复制颈总动脉球囊损伤模型,分离颈总动脉制备病理切片,HE染色观察内膜增生情况.免疫组化观察增殖、迁移相关蛋白表达情况.贴块法培养血管平滑肌细胞(VSMC),待生长至70％～ 80％融合时,分别加入不同浓度苯磺酸氨氯地平,继续孵育24 h,细胞计数及Western印迹法用于分析VSMC增殖活性;伤口愈合实验及明胶酶图实验用于分析VSMC迁移活性.结果 AM抑制球囊损伤诱导的血管新生内膜形成和管腔狭窄,与AT联用增强其抑制效果;AM单独及与AT联合用药抑制球囊损伤诱导的PCNA、KLF5、MMP-9 的表达;AM抑制体外培养的VSMC中PCNA、KLF5和c-Jun的表达;降低MMP-2和MMP-9的活性.结论 AM抑制球囊损伤诱导的血管新生内膜形成与其抑制VSMC增殖及迁移活性有关. 相似文献
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