Abstract：
Smoking is a well-established risk factor for several oral diseases, including oral cancer, oral leukoplakia and periodontitis, primarily related to reactive oxygen species (ROS). SS-31, a mitochondria-targeting tetrapeptide, has exhibited demonstrable efficacy in medical conditions by attenuating mitochondrial ROS production. However, its potential in the treatment of oral diseases remains underexplored. The aim of this study was to investigate the therapeutic potential of SS-31 in mitigating smoking-induced oral epithelial injury. Through in vitro experiments, our results indicate that SS-31 plays a protective role against cigarette smoke extract (CSE) by reducing oxidative stress, attenuating inflammatory response, and restoring mitochondrial function. Furthermore, we found that mitophagy, regulated by PINK1 (PTEN-induced putative kinase 1)/Parkin (Parkin RBR E3 ubiquitin-protein ligase), was critical for the protective role of SS-31. Our findings offer valuable insights into SS-31\'s therapeutic potential in mitigating CSE-induced oxidative stress, inflammatory response, and mitochondrial dysfunction in oral epithelial cells. This study provides novel intervention targets for smoking-related oral diseases.
摘要：
吸烟是几种口腔疾病的公认危险因素，包括口腔癌,口腔白斑和牙周炎，主要与活性氧（ROS）有关。SS-31，一种线粒体靶向四肽，通过减弱线粒体ROS的产生，在医疗条件下表现出明显的疗效。然而,其在口腔疾病治疗中的潜力仍未得到充分开发。这项研究的目的是研究SS-31减轻吸烟引起的口腔上皮损伤的治疗潜力。通过体外实验,我们的结果表明，SS-31通过减少氧化应激发挥对香烟烟雾提取物（CSE）的保护作用，减弱炎症反应，恢复线粒体功能.此外，我们发现有丝分裂自噬,由PINK1（PTEN诱导的推定激酶1）/Parkin（ParkinRBRE3泛素蛋白连接酶）调节，对SS-31的保护作用至关重要。我们的发现为SS-31在缓解CSE诱导的氧化应激方面的治疗潜力提供了有价值的见解。炎症反应，口腔上皮细胞线粒体功能障碍。这项研究为吸烟相关的口腔疾病提供了新的干预目标。
