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中文摘要：
目的：探讨吡格列酮对间歇性低氧大鼠氧化应激与胰岛素抵抗的干预作用。方法：建立OS-AHS模型，将SD雄性大鼠36只随机分为常氧对照组、模型组、吡格列酮干预组，每组12只。干预组给予吡格列酮10ml·kg-1·d-1灌胃，模型、对照组均予等量生理盐水灌胃。于实验8周终点处死大鼠，硫代巴比妥酸法、酶联免疫吸附法、比色法、蛋白免疫印迹等方法观察各组大鼠血清TNF-α、MDA、GsH-Px、H（JMA-IR及胰腺组织NF-KB蛋白的表达情况。结果：与对照组比较，模型、干预组大鼠血清TNF-α、MDA、FBG、FlNS、HOMA-IR及胰腺组织NF-KB蛋白表达均升高，GSH-Px水平降低（P〈O．05）；与模型组比较，干预组血清TNF-α、MDA、FBG、FINS、HOMA-IR及胰腺组织NF-KB蛋白表达均降低，GSH-Px水平升高（P〈0．05）。结论：吡格列酮可通过抑制NF-κB核转位降低慢性间歇行低氧氧化应激水平，改善胰岛素抵抗状态。
英文摘要：
Objective： To investigate the intervention effect of pioglitazone on the oxidative stress lev el and insulin resistance of chronic intermittent hypoxia rats. Methods： Obstructive sleep aponea- hypopnea syndrorne（OSAHS） models in rats were established. 36 male Sprague-Dawley（SD） rats were randomized into 3 groups： the normoxic control group, the model group, and the pioglitazone intervention group. Each group had 12 rats. Rats in the intervention group were gavaged with piogl- itazone （10 ml·kg-1·d-1）, and those in the model and control group were treated with isovalent normal saline by gavage. The rats were sacrificed at the end of 8 weeks and changes were detected a.bout the serum TNF-α, MDA, GSH-Px, FBG, FINS, HOMA-IR, and the expression of, pancreas tissue NF-κB protein as well by TBA test, ELISA, colorimetry and western blotting. Results： Compared with the control group, the serum TNF-a, MDA, FBG, FINS, HOMA-IR, and the ex pression of pancreas tissue NF-κB protein in the model and intervention group increased, while GSH-Px level declined（P〈0.05）; Compared with the model group, the serum TNF-a, MDA, FBG, FINS, HOMA-IR and pancreas tissue NF-κB protein expression in the intervention rats declined, while GSH-Px level rised（P〈0.05）. Conclusion： Pioglitazone can degrade the oxidative stress level and improve the insulin resistance state in chronic intermittent hypoxia rats through inhibiting the NF-κB translocation.
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