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抗FAS抗体诱导软骨细胞凋亡及胰岛素样生长因子-1对其的保护作用

期刊名称：中国骨科杂志
时间：0
页码：920-924
语言：中文
分类：R68[医药卫生—骨科学;医药卫生—临床医学;医药卫生—外科学] R684.302[医药卫生—骨科学;医药卫生—临床医学;医药卫生—外科学]
作者机构：[1]上海中医药大学附属龙华医院脊柱病研究所,200032, [2]香港大学医学院骨科学系
相关基金：国家杰出青年科学基金资助项目（30625043）;国家自然科学基金重点资助项目（30330700）;国家自然科学基金资助项目（30371794,30171170＆30572398）;上海市科技“启明星”跟踪计划（05QMHl412）;上海市“曙光学者”计划（05SG44）;上海市医学重点学科建设项目（051027）;上海市重点学科建设项目（T0303）
相关项目：中医骨伤科学

关键词：软骨细胞, 细胞凋亡, 胰岛素样生长因子I, Chondrocytes, Apoptosis, Insulin-like growth factor I

中文摘要：

目的建立抗Fas抗体诱导大鼠终板软骨细胞凋亡模型，检测胰岛素样生长因子-l（insulin-like growth factor-1，IGF-1）是否有延缓软骨细胞凋亡的作用，并进一步了解软骨细胞中整合素βl和黏着斑激酶（focal adhesion kinase，FAK）的表达情况。方法取大鼠颈椎软骨终板软骨细胞行体外培养，应用抗Fas抗体（500ng／ml）和人重组IGF—l（50ng／ml）处理。光学显微镜观察细胞形态，透射电子显微镜、TUNEL法观察软骨细胞凋亡形态，免疫细胞化学法检测Bax、Bcl-2表达，实时荧光定量聚合酶链反应、免疫细胞化学和Western blot法检测整合素βl和FAK的基因与蛋白表达。结果体外培养出软骨细胞并维持其表型。抗Fas抗体诱导软骨细胞发生凋亡，TUNEL染色证明软骨细胞凋亡率升高，透射电镜检查发现典型凋亡小体。与正常组比较，诱导凋亡组Bcl-2表达降低而Bax表达升高，整合素βl和FAK的基因与蛋白表达明显下调；抗Fas抗体与IGF-I联合干预后，Bcl-2表达升高而Bax表达降低，整合素βl和FAK的基因与蛋白表达明显上调。结论抗Fas抗体可诱导体外培养的终板软骨细胞凋亡，抗Fas抗体与IGF-I联合应用，能延缓软骨细胞凋亡的过程，维持软骨细胞的功能。

英文摘要：

Objective In vitro investigation chondrocytes apoptosis by anti-Fas antibody-induced in cultured endplate chondrocytes, and whether treatment with insulin-like growth factor-I （IGF-I） blocked these effects. The expression of the extracellular matrix proteins integrin-β1 and focal adhesion kinase （FAK） in conjunction with apoptosis was also investigated. Methods Rat cervical endplate chondrocytes were cultured and treated with anti-Fas antibody, with or without human recombinant IGF-I. Cellular morphology was examined by light microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining of Bax and Bcl-2. Apoptosis induced changes in the expres- sion of integrin-β1 and FAK were investigated using real time polymerase chain reaction, immunostaining and Western blot. Results Endplate chondrocytes were able to be cultured, with maintenance of a chondrocytic phenotype. Anti-Fas antibody induced apoptotic changes in endplate chondrocytes. TUNEL staining confirmed increased apoptosis in antibody treated ceils. Expression of Bcl-2 was decreased by anti-Fas antibody, while expression of Bax was increased. Expression of integrin-β1 and FAK were decreased by antiFas antibody treatment. Co-treatment with IGF-I rescued cells from these anti-Fas antibody-induced changes. Conclusion Anti-Fas antibody induces apoptosis of cultured endplate chondrocytes. IGF-1 protects these chondrocytes from anti-Fas antibody-induced apoptosis, and IGF-I inhibited expression of integrin-β1 and FAK. It can delay the process which the chondrocytes apoptosis and maintenance these cells function condition.

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