中国病理生理杂志2016，Vol.32Issue(11)：2036-2042,7.DOI:10.3969/j.issn.1000-4718.2016.11.020
晚期糖基化终末产物通过氧化应激诱导大鼠软骨细胞损伤∗
Advanced glycation end products induce rat chondrocyte injury by modu-lating oxidative stress
摘要
Abstract
AIM: To explore the possibility that advanced glycation end products (AGEs) induces rat chon-drocyte injury by modulating oxidative stress. METHODS:Primarily cultured rat chondrocytes were identified. The viabil-ity of the chondrocytes was measured by CCK-8 assay. The intracellular levels of reactive oxygen species ( ROS) were de-tected 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. CON-CLUSION:AGEs induce chondrocyte injury by activating oxidative stress.关键词
晚期糖基化终末产物/骨性关节炎/氧化应激/基质金属蛋白酶/细胞凋亡Key words
Advanced glycation end products/Osteoarthritis/Oxidative stress/Matrix metalloproteinases/Apoptosis分类
医药卫生引用本文复制引用
黄文舟,王丽丽,殷嫦嫦,李健,敖鹏,程细高..晚期糖基化终末产物通过氧化应激诱导大鼠软骨细胞损伤∗[J].中国病理生理杂志,2016,32(11):2036-2042,7.基金项目
国家自然科学基金资助项目(No.81060147) （No.81060147）
