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作 者:王红林[1] 王治伦[1] 陈静宏[1] 吴劲[1] 考希宾[1] 高艳[1]
机构地区:[1]西安交通大学医学院地方病研究所环境与疾病相关基因教育部重点实验室,陕西西安710061
出 处:《西安交通大学学报(医学版)》2007年第5期537-539,558,共4页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:国家自然科学基金资助项目(No.30371245No.39770667)
摘 要:目的探讨p38 MAPK抑制剂SB203580对软骨细胞NF-κB蛋白表达的影响。方法体外培养兔关节软骨细胞,经甲苯胺兰染色鉴定后,一氧化氮(NO)供体NOC-18和p38 MAPK抑制剂SB203580作用于细胞24 h,用MTT比色法检测细胞增殖活性,Western blot测定NF-κB p65亚单位蛋白表达水平。结果与对照组比较,NOC-18能抑制软骨细胞MTT增殖活性(P<0.05);NOC-18诱导的NF-κB p65活性的升高被SB203580抑制(P<0.05),而仅有SB203580作用于细胞时,与对照组比较,差别无统计学意义(P>0.05)。结论p38 MAPK促进了NO诱导的兔关节软骨细胞NF-κB的表达,NO致软骨细胞凋亡的信号通路中涉及了NF-κB的活性表达。Objective To explore the effect of p38 MAPK inhibitor SB203580 on chondrocyte protein expression of NF-κB. Methods Rabbit articular chondrocytes were cultured in vitro, and identified using toluidine blue staining. Following treatment with nitric oxide (NO) donor NOC-18 and p38 MAPK inhibitor SB203580 for 24 h, we performed MTT assay to evaluate the proliferation of cells, and Western blotting to determine the protein expression of NF-κB p65. Results NOC-18 significantly reduced chondrocyte proliferation, compared with untreated controls (P〈0.05); SB203580 was able to suppress the accelerated activity of NF-κB p65 induced by NOC-18 (P〈0.05). However, there was no significant difference when treated only with SB203580, compared with the control (P 〉 0. 05). Conclusion The p38 MAPK promotes NO-induced rabbit articular chondrocyte NF-κB expression, and the increase of NF-κB expression is involved in NO-induced chondrocyte apoptosis pathway.
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