Advanced glycation end products induce rat chondrocyte injury by modulating oxidative stress |
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| Authors: | HUANG Wen-zhou WANG Li-li YIN Chang-chang LI Jian AO Peng CHENG Xi-gao |
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| Institution: | 1. Department of Orthopedics, The Second Affiliated Hospital of Nanchang University, Nanchang 330006;
2. Jiujiang University, Key Laboratory of Medical Trans formation of Jiujiang, Jiujiang 332000, China |
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| Abstract: | ATM: 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. |
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| Keywords: | Advanced glycation end products Osteoarthritis Oxidative stress Matrix metalloproteinases Apoptosis |
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