中文摘要：

目的：探讨晚期糖基化终末产物（advanced glycation end products,AGEs）能否通过氧化应激引起大鼠软骨细胞损伤。方法：原代培养SD大鼠软骨细胞,对细胞表型进行鉴定;应用CCK-8法检测软骨细胞生存率;DCFH-DA染色荧光显微镜下检测胞内活性氧簇（reactive oxygen species,ROS）的水平;Hoechst 33342核染色法及Annexin V-FITC/PI流式细胞法测定软骨细胞的凋亡率;RT-PCR法检测软骨细胞中Bax、Bcl-2、caspase-3、MMP3、MMP13和COL2的mRNA水平;Western blotting法检测软骨细胞中cleaved caspase-3、MMP3、MMP13和COL2的蛋白水平。结果：与对照组相比,AGEs可显著上调胞内ROS水平（P〈0.05）,但经抗氧化剂N-乙酰半胱氨酸（NAC）抑制后ROS的生成明显减少（P〈0.05）;另外,NAC可抑制AGEs引起的软骨细胞凋亡相关分子Bax/Bcl-2和caspase-3水平的上调,并减少MMP3和MMP13表达及COL2的丢失（P〈0.05）。结论：AGEs可通过氧化应激诱导大鼠软骨细胞损伤。

英文摘要：

AIM： To explore the possibility that advanced glycation end products（ AGEs） induces rat chondrocyte injury by modulating oxidative stress. METHODS： Primarily cultured rat chondrocytes were identified. The viability of the chondrocytes was measured by CCK-8 assay. The intracellular levels of reactive oxygen species（ ROS） were detected by DCFH-DA staining. The number of apoptotic cells was determined by Hoechst 33342 nuclear staining and flow cytometry. RT-PCR was performed to measure the mRNA levels of Bax,Bcl-2,caspase-3,MMP3,MMP13 and COL2 in the chondrocytes. Western blotting was used to evaluate the protein levels of cleaved caspase-3,MMP3,MMP13 and COL2. RESULTS： Compared with control group,the intracellular levels of ROS in the chondrocytes treated with AGEs were significantly increased（ P〈0. 05）,and pretreatment with N-acetyl-L-cysteine（ NAC） suppressed the formation of ROS（ P〈0. 05）. Besides,NAC inhibited AGEs-induced apoptosis of the chondrocytes,as indicated by reduceing the levels of Bax / Bcl-2 and caspase-3,decreased the expression of MMP3 and MMP13,and reduced the loss of COL2. CONCLUSION： AGEs induce chondrocyte injury by activating oxidative stress.