Ding W X, Zhang Q, Ge L Y, Dong Y B, Ding N, Zhang X L
Department of Respirology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, China.
Department of Respirology and Critical Care Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Zhonghua Yi Xue Za Zhi. 2019 May 14;99(18):1380-1384. doi: 10.3760/cma.j.issn.0376-2491.2019.18.005.
To explore the effect of adiponectin (APN) on islet injury induced by chronic intermittent hypoxia (CIH). Thirty-six SD rats were randomly divided into three groups: Normal control (NC), CIH, and CIH + APN groups. The rats in the CIH and CIH+APN groups received an intermittent hypoxia exposure while the rats in NC group received the room air only. The rats in CIH+APN group received the intravenous injection of APN. The intermittent hypoxia events persisted 8 hours a day and last for 35 days. The fasting blood glucose and fasting insulin were detected at the time of 0, 7, 14, 21, 28, and 35 day. After 35 days, the level of serum adiponectin, and adenosine triphosphate (ATP) level, superoxide dismutase (SOD), malondialdehyde (MDA), the mRNA levels of mitochondrial oxidative phosphorylation function and mitochondrial synthesis gene, and the protein level of mitochondrial and cytoplasmic cytochrome C of pancreatic islet were detected. The glucose and insulin level had no statistically differences among three groups at different time points (all 0.05). However, compared with NC and CIH+APN groups, CIH reduced the serum adiponectin [(7 265±2 209) ng/ml, (6 536±1 678) ng/ml vs (4 923±1 742) ng/ml, both 0.05], ATP levels [(30.92±1.12) nmol/mg, (26.55±0.72) nmol/mg vs (20.22±1.47) nmol/mg, both 0.05], mRNA levels of mitochondria oxidative phosphorylation function and mitochondrial synthesis gene, the activity of SOD, and the rate of mitochondrial/cytoplasmic cytochrome C protein level while increased the MDA level in pancreatic islet. Compared with NC group, the MDA level increased (0.05) and the APN level had no statistically difference, while the level of other indicators decreased in CIH+APN group (all 0.05). APN ameliorates the pancreatic islet injury induced by CIH through inhibition of oxidative stress.
探讨脂联素（APN）对慢性间歇性缺氧（CIH）诱导的胰岛损伤的影响。将36只SD大鼠随机分为三组：正常对照组（NC）、CIH组和CIH + APN组。CIH组和CIH + APN组大鼠接受间歇性缺氧暴露，而NC组大鼠仅接受室内空气。CIH + APN组大鼠接受静脉注射APN。间歇性缺氧事件每天持续8小时，持续35天。在第0、7、14、21、28和35天检测空腹血糖和空腹胰岛素。35天后，检测血清脂联素水平、三磷酸腺苷（ATP）水平、超氧化物歧化酶（SOD）、丙二醛（MDA）、线粒体氧化磷酸化功能和线粒体合成基因的mRNA水平以及胰岛线粒体和细胞质细胞色素C的蛋白水平。三组在不同时间点的血糖和胰岛素水平无统计学差异（均P>0.05）。然而，与NC组和CIH + APN组相比，CIH组降低了血清脂联素水平[（7 265±2 209）ng/ml，（6 536±1 678）ng/ml比（4 923±1 742）ng/ml，均P<0.05]、ATP水平[（30.92±1.12）nmol/mg，（26.55±0.72）nmol/mg比（20.22±1.47）nmol/mg，均P<0.05]、线粒体氧化磷酸化功能和线粒体合成基因的mRNA水平、SOD活性以及线粒体/细胞质细胞色素C蛋白水平比例，同时增加了胰岛中的MDA水平。与NC组相比，CIH + APN组MDA水平升高（P<0.05）且APN水平无统计学差异，而其他指标水平降低（均P<0.05）。APN通过抑制氧化应激改善CIH诱导的胰岛损伤。
