脂联素缓解慢性间歇低氧所致的颏舌肌线粒体损伤

Adiponectin alleviates genioglossal mitochondrial injury induced by chronic intermittent hypoxia in rats

摘要:

目的 探讨慢性间歇低氧（CIH）对颏舌肌线粒体的损伤以及脂联素（Ad）的干预作用及机制。方法 45只成年Wistar大鼠随机分为3组：正常对照（NC）组、CIH组及CIH＋Ad组，每组15只。CIH组及CIH＋Ad组的大鼠暴露于同样的间歇低氧环境（8h/d，5周），而NC组的大鼠则只暴露于正常空气。此外，CIH＋Ad组的大鼠还接受2次/周的Ad静脉注射。结果 与NC组相比，CIH组大鼠的颏舌肌出现以下的损伤性表现：线粒体数量减少、线粒体结构损伤伴Ⅰ型纤维减少（P＜0.05）。但与CIH组相比，CIH＋Ad组的大鼠颏舌肌线粒体结构和功能改善且Ⅰ型纤维的数量有所增加（P＜0.05）。与NC组相比，CIH组大鼠颏舌肌显示LKB1-AMPK-PGC1-α通路蛋白表达下降（P＜0.05），而CIH＋Ad组较CIH组有明显改善（P＜0.05）。结论 CIH可引起颏舌肌线粒体等损伤，而补充外源性Ad可能通过调节AMPK通路改善上述CIH诱导的颏舌肌病理改变。

Abstract:

Objective To determine the effects of chronic intermittent hypoxia (CIH) on the injury in genioglossal mitochondria and investigate the intervention role of adiponectin (Ad) in the process and associated mechanisms. Methods Forty-five adult Wistar rats were randomly divided into 3 groups, that is, normal control (NC) group, CIH group, and CIH＋Ad group, with 15 rats in each group. The rats in the 2 latter groups were exposed to the same CIH environment (8h/d for 5 weeks), while the rats in the NC group were exposed to normal air only. In addition, the rats in CIH＋Ad group were injected with Ad (10μg, twice a week). Results Compared with the NC group, reduced amount, damaged structure and decreased type Ⅰ fibers in the genioglossal mitochondria were observed in the rats of CIH group (P＜0.05). However, the conditions in the rats of CIH＋Ad group were much better (P＜0.05). Compared with the NC group, the protein expression of LKB1-AMPK-PGC1-α pathway was significantly lower in the genioglossum of CIH group, but such a reduction was less significant in CIH＋Ad group (P＜0.05). Conclusion CIH induces impairment in genioglossal mitochondria, while supplement of Ad will improve such genioglossal injuries possibly via modulation of AMPK pathway.