{"title":"Effects of Mandibular Advancement Device on Genioglossus of Rabbits in Obstructive Sleep Apnea Through PINK1/Parkin Pathway.","authors":"Lishuang Ma, Yahui Zhu, Zuo Zhang, Dengying Fan, Haoyan Zhai, Dongna Li, Wenjing Kang, Xing Qiao, Haiyan Lu, Chunyan Liu","doi":"10.1111/joor.13907","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Early treatment of mandibular advancement device (MAD) reverses the abnormal changes resulting from obstructive sleep apnoea (OSA), but the underlying mechanism is not clear. We analysed the changes of genioglossus function before and after MAD treatment in OSA rabbits and explored the mechanism of mitochondrial autophagy.</p><p><strong>Methods: </strong>Eighteen male New Zealand rabbits were randomised into three groups: the control group, Group OSA, and Group MAD. After successful modelling, all animals were induced sleep in supine positions for 4-6 h per day for 8 weeks. Cone beam computed tomography (CBCT) and polysomnography (PSG) were performed to record sleep conditions. The genioglossus contractile force and the levels of LC3-I, LC3-II, Beclin-1, PINK1 and Parkin were detected in three groups. In vitro, C2C12 myoblast cells were cultured under normoxic or hypoxic conditions for 24 h, and then the changes in mitochondrial structure and accumulation of autolysosomes were detected by transmission electron microscopy (TEM).</p><p><strong>Results: </strong>The contractile tension of the genioglossus in Group OSA was significantly lower than that in the control group. The ratio of LC3II/LC3I and the levels of Beclin-1, PINK1 and Parkin were higher in Group OSA than that in the control group. And the abnormal changes were tended to be normal after MAD treatment. The mitochondrial structure was disrupted, and the number of autolysosomes increased in C2C12 after 24 h of hypoxia.</p><p><strong>Conclusions: </strong>MAD treatment in male rabbits may decrease the contractile tension of the genioglossus and increase the level of mitochondrial autophagy caused by OSA. And the mechanism of mitochondrial autophagy was mediated by the PINK1/Parkin pathway in male rabbits.</p>","PeriodicalId":16605,"journal":{"name":"Journal of oral rehabilitation","volume":" ","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of oral rehabilitation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/joor.13907","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Early treatment of mandibular advancement device (MAD) reverses the abnormal changes resulting from obstructive sleep apnoea (OSA), but the underlying mechanism is not clear. We analysed the changes of genioglossus function before and after MAD treatment in OSA rabbits and explored the mechanism of mitochondrial autophagy.
Methods: Eighteen male New Zealand rabbits were randomised into three groups: the control group, Group OSA, and Group MAD. After successful modelling, all animals were induced sleep in supine positions for 4-6 h per day for 8 weeks. Cone beam computed tomography (CBCT) and polysomnography (PSG) were performed to record sleep conditions. The genioglossus contractile force and the levels of LC3-I, LC3-II, Beclin-1, PINK1 and Parkin were detected in three groups. In vitro, C2C12 myoblast cells were cultured under normoxic or hypoxic conditions for 24 h, and then the changes in mitochondrial structure and accumulation of autolysosomes were detected by transmission electron microscopy (TEM).
Results: The contractile tension of the genioglossus in Group OSA was significantly lower than that in the control group. The ratio of LC3II/LC3I and the levels of Beclin-1, PINK1 and Parkin were higher in Group OSA than that in the control group. And the abnormal changes were tended to be normal after MAD treatment. The mitochondrial structure was disrupted, and the number of autolysosomes increased in C2C12 after 24 h of hypoxia.
Conclusions: MAD treatment in male rabbits may decrease the contractile tension of the genioglossus and increase the level of mitochondrial autophagy caused by OSA. And the mechanism of mitochondrial autophagy was mediated by the PINK1/Parkin pathway in male rabbits.
期刊介绍：
Journal of Oral Rehabilitation aims to be the most prestigious journal of dental research within all aspects of oral rehabilitation and applied oral physiology. It covers all diagnostic and clinical management aspects necessary to re-establish a subjective and objective harmonious oral function.
Oral rehabilitation may become necessary as a result of developmental or acquired disturbances in the orofacial region, orofacial traumas, or a variety of dental and oral diseases (primarily dental caries and periodontal diseases) and orofacial pain conditions. As such, oral rehabilitation in the twenty-first century is a matter of skilful diagnosis and minimal, appropriate intervention, the nature of which is intimately linked to a profound knowledge of oral physiology, oral biology, and dental and oral pathology.
The scientific content of the journal therefore strives to reflect the best of evidence-based clinical dentistry. Modern clinical management should be based on solid scientific evidence gathered about diagnostic procedures and the properties and efficacy of the chosen intervention (e.g. material science, biological, toxicological, pharmacological or psychological aspects). The content of the journal also reflects documentation of the possible side-effects of rehabilitation, and includes prognostic perspectives of the treatment modalities chosen.
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