Hydroxytyrosol prevents periodontitis-induced bone loss by regulating mitochondrial function and mitogen-activated protein kinase signaling of bone cells.
Hydroxytyrosol prevents periodontitis-induced bone loss by regulating mitochondrial function and mitogen-activated protein kinase signaling of bone cells.
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DOI：
10.1016/j.freeradbiomed.2021.09.027
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发表时间：
2021-10
影响因子：
7.4
通讯作者：
Xiaorong Zhang;Yun Jiang;Jiajie Mao;Xuekun Ren;Yinghui Ji;Y. Mao;Yang Chen;Xiaoyu Sun;Yihuai Pan;Jianfeng Ma;Sheng-Bing Huang
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文献类型：
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作者：
Xiaorong Zhang;Yun Jiang;Jiajie Mao;Xuekun Ren;Yinghui Ji;Y. Mao;Yang Chen;Xiaoyu Sun;Yihuai Pan;Jianfeng Ma;Sheng-Bing Huang
牙周炎发生发展过程中，活性氧（ROS）的过量产生促进了牙槽骨的丢失。线粒体是ROS的主要来源。羟基酪醇（HT）是一种存在于橄榄油中的天然酚类化合物，以其抗氧化和保护生殖器官的特性而闻名。然而，HT对牙周炎的影响及其相关的骨细胞行为机制仍不清楚。用HT和不用HT处理从RAW264.7模型和氧化应激（OS）诱导的前成骨细胞MC 3 T3-E1细胞损伤模型分化的破骨细胞。研究细胞活力、凋亡、分化、线粒体功能沿着丝裂原活化蛋白激酶（MAPK）信号通路。同时，观察HT对牙周炎小鼠骨丢失的影响及相关机制。HT通过调节线粒体功能以及ERK和JNK信号通路抑制破骨细胞分化，防止OS诱导的前成骨细胞损伤。HT还能减轻牙周炎小鼠牙槽骨丢失，增加骨形成活性，抑制破骨细胞分化，降低骨代谢水平。我们的研究结果，首次揭示了一个新的功能，HT在牙周炎的骨改建，并强调其治疗牙周炎的预防/治疗的潜力。
Reactive oxygen species (ROS) overproduction promotes the alveolar bone loss during the development of periodontitis. Mitochondria are the principal source of ROS. Hydroxytyrosol (HT), a natural phenolic compound present in olive oil, is well known for its antioxidant and mitochondrial-protective prosperities. Nonetheless, the impact of HT on periodontitis and its related mechanisms underlying bone cell behavior remains unknown. Osteoclasts differentiated from RAW264.7 model and oxidative stress (OS) induced pre-osteoblast MC3T3-E1 cell injury model were treated with and without HT. Cell viability, apoptosis, differentiation, mitochondrial function along with mitogen-activated protein kinase (MAPK) signaling pathway were investigated. Meanwhile, the effect and related mechanisms of HT on bone loss in mice with periodontitis were also detected. HT inhibited osteoclast differentiation and prevented OS induced pre-osteoblast cells injury via regulating mitochondrial function as well as ERK and JNK signaling pathways. Moreover, HT attenuated the alveolar bone loss, increased bone forming activity, inhibited the osteoclasts differentiation and decreased the level of OS in mice with periodontitis. Our findings,for the first time, revealed a novel function of HT in bone remodeling of periodontitis, and highlighted its therapeutical potential for the prevention/treatment of periodontitis.