Ogg1 protects against the catabolic stress-induced downregulation of chondrocyte activity and the apoptosis in OA.

众所周知，软骨细胞产生过量的活性氧（ROS）以及促炎细胞因子和趋化因子，以响应机械和化学应力。鸟嘌呤的氧化形式8-氧代-7，8-二羟基鸟嘌呤（8-oxoguanine）是ROS诱变的主要致病性损伤，因为它可以在DNA复制过程中与腺嘌呤或胞嘧啶形成稳定的碱基对。8-氧代鸟嘌呤DNA糖基化酶（Ogg 1）修复8-氧代鸟嘌呤，氧自由基引起的最丰富的DNA加合物之一。我们证明了骨关节炎软骨细胞中细胞抗氧化剂Ogg 1的耗竭参与了OA关节软骨的退化。我们的研究结果表明，Ogg 1可能有潜力，以防止分解代谢因子诱导的下调软骨细胞活性和凋亡的OA。

It is well known that chondrocytes produce excess amounts of reactive oxygen species (ROS) as well as proinflammatory cytokines and chemokines in response to mechanical and chemical stresses. An oxidized form of guanine, 8-oxo-7,8-dihydroxyguanine (8-oxoguanine), is a major causative lesion for mutagenesis by ROS, because it can cause a stable base pair with adenine or cytosine during DNA replication. 8-Oxoguanine DNA glycosylase (Ogg1) repairs 8-oxoguanine, one of the most abundant DNA adducts caused by oxygen free radicals. We demonstrated that depletion of cellular antioxidant, Ogg1, in osteoarthritic chondrocytes participates in the degeneration of articular cartilage in OA. Our findings suggest that Ogg1 may have a potential to protect against the catabolic factor-induced down-regulation of chondrocyte activity and apoptosis in OA.