All methods in this study were performed in accordance with the medical ethics committee in Hospital of Stomatology, Hebei Medical University. Animal use and care was in accordance with the guidelines of the medical ethics committee for the housing and care of animals bred, supplied and used for scientific purposes. All experiments were performed in accordance with relevant guidelines and regulations. The work was approved by the medical ethics committee in Hospital of Stomatology, Hebei Medical University (Certificate No. [2017]016). Animal model development. Every effort was made to minimize animal pain and suffering. A total of 18 male 6-month-old New Zealand white rabbits (initial weight, 3-3.5 kg) were randomly divided into three groups: the OSHAS, MAD, and control groups, with 6 rabbits in each group. All of the animals were housed under normal laboratory conditions. Food and water were available ad libitum. The animal models were developed in the same way as in our previous studies 12,13. Briefly, OSAHS was induced via injection of gel into the submucous muscular layer in the centre of the soft palate 1.5 cm away from the junction of the soft and hard palate (Fig. 1). No gel was injected in the control group. Animals in these two groups were later confirmed to have OSAHS by clinical signs, CBCT scanning and polysomnography (PSG).
Background: To examine the morphology and function of mitochondria from the genioglossus in a rabbit model of obstructive sleep apnea-hypopnea syndrome (OSAHS), as well as these factors after insertion of a mandibular advancement device (MAD). Methods: Thirty male New Zealand white rabbits were randomized into three groups: control, OSAHS and MAD, with 10 rabbits in each group. Animals in Group OSAHS and Group MAD were induced to develop OSAHS by injection of gel into the submucosal muscular layer of the soft palate. The rabbits in Group MAD were fitted with a MAD. The animals in the control group were not treated. Further, polysomnography (PSG) and CBCT scan were used to measure MAD effectiveness. CBCT of the upper airway and PSG suggested that MAD was effective. Rabbits in the three groups were induced to sleep for 4–6 hours per day for 8 consecutive weeks. The genioglossus was harvested and detected by optical microscopy and transmission electron microscopy. The mitochondrial membrane potential was determined by laser confocal microscopy and flow cytometry. Mitochondrial complex I and IV activities were detected by mitochondrial complex assay kits.Results: OSAHS-like symptoms were induced successfully in Group OSAHS and rescued by MAD treatment. The relative values of the mitochondrial membrane potential, mitochondrial complex I activity and complex IV activity were significantly lower in Group OSAHS than in the control group; however, there was no significant difference between Group MAD and the control group. The OSAHS-induced injury and the dysfunctional mitochondria of the genioglossus muscle were reduced by MAD treatment.Conclusion: Damaged mitochondrial structure and function were induced by OSAHS and could be attenuated by MAD treatment.
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