中文摘要：

目的 探讨p38 MAPK信号转导通路在软骨细胞凋亡中的作用。方法 体外培养兔关节软骨细胞，一氧化氮（NO）供体NOC-18和p38MAPK抑制剂SB203580作用于细胞24h，用Annexin V-FITC／PI流式细胞术检测软骨细胞凋亡率，Western blot测定p38、磷酸化p38蛋白的表达水平。结果 与对照组比较，SB203580显著降低了NOC-18诱导的软骨细胞凋亡率（P〈0．05）；NOC-18以浓度依赖的方式促进p38MAPK的磷酸化，而SB203580能抑制其磷酸化（P〈0.05）。结论 p38MAPK通路参与了NO诱导的兔关节软骨细胞凋亡的信号转导。

英文摘要：

Objective To explore the role of p35 MAPK signal transduction pathway in chondrocyte apoptosis. Methods Rabbit articular chondrocytes were cultured in vitro. Following treatment with NO donor NOC - 18 and p38 MAPK inhibitor SB203580 for 24 h, we performed Annexin V - FITC/PI flow cytometry （FCM） to detect chondrocyte apoptosis rate, and Western blotting to determine the protein expression of p38, phosphorylation p38. Results SB203580 significantly decreased chondrocyte apoptosis rate, compared with untreated control （ P 〈0. 05） ; NOC -18 promoted the phosphorylation of p38 MAPK in a concentration - dependent manner, and SB203550 could inhibit it （ P 〈 0. 05）. Conclusions The p38 MAPK pathway is involved in the signal transduction of NO - induced rabbit articular chondrocyte apoptosis.