中文摘要：

目的：探讨自噬在慢性间歇性低氧状态下大鼠颏舌肌损伤中的作用及其机制。方法：将36只SD大鼠随机均分为对照组,慢性间歇性低氧组（chronic intermittent hypoxia,CIH组）,慢性间歇性低氧＋氯喹组（CIH＋CQ组）。苏木素-伊红（HE）染色观察颏舌肌组织形态学变化;激光共聚焦显微镜下观察自噬标记物LC3在颏舌肌中的表达;免疫组织化学染色法观察组织中细胞色素c（cytochrome,Cyt c）的表达。结果：激光共聚焦结果显示,对照组颏舌肌中未见明显LC3表达,CIH组中LC3的平均荧光强度较对照组明显增强（P〈0.05）,CIH＋CQ组中LC3的平均荧光强度较CIH组显著增加（P〈0.05）。免疫组织化学结果显示：CIH组中Cyt c的阳性表达较对照组增加（P〈0.05）,CIH＋CQ组中Cyt c表达与CIH组相比显著增加（P〈0.05）。结论：慢性间歇性低氧引起颏舌肌线粒体损伤,触发细胞凋亡,同时诱发自噬。抑制自噬加重线粒体损伤,促进细胞凋亡。说明自噬可能通过抑制凋亡而在慢性间歇性低氧状态下的大鼠颏舌肌中起维护肌肉功能的作用。

英文摘要：

Objective： To explore the effect and mechanism of autophagy on rats genioglossus muscle injury caused by chronic intermittent hypoxia. Methods： 36 SD rats were randomly divided into three groups, control group, chronic intermittent hypoxia group （CIH group） and chronic intermittent hypoxia plus chloroquine group （CIH＋CQ group）. The morphological changes of genioglossus muscle were observed by HE staining. Laser confocal microscopy was used to observe the expression of LC3 protein. Immunohistochemistry was used to observe the expression of Cyt c protein. Results： There is no obvious expression of LC3 and Cyt c protein in control group. In C1H group, the mean fluorescence intensity of LC3 and the positive rate of Cyt c were higher than that in control group （P〈0.05）. In CIH＋CQ group, the mean fluorescence intensity of LC3 and the positive rate of Cyt c apparently increased compared with that in CIH group（P〈0.05 ）. Conclusions： Chronic intermittent hypoxia may cause mitochondrial damage and trigger early apoptosis in genioglossus muscle. Meanwhile, it can induce the autophagy in genioglossus muscle. Inhibition of autophagy may aggravate the mitochondrial damage and promote apoptosis. This suggests that autophagy may protect genioglossus muscle from the damage which caused by chronic intermittent hypoxia through inhibiting apoptosis.