【摘要】：目的探討單磷酸腺苷激活蛋白激酶(AMPK)活化對(duì)慢性間歇缺氧大鼠胰島素抵抗和炎癥因子的作用及其機(jī)制。方法建立慢性間歇缺氧大鼠模型模擬阻塞性睡眠呼吸暫停綜合征(OSAS),將36只雄性SD大鼠分為常氧對(duì)照組、2周間歇缺氧組、8周間歇缺氧組。觀察AMPK激動(dòng)劑和AMPK抑制劑作用不同缺氧程度的大鼠體內(nèi)炎癥介質(zhì)、血脂、脂聯(lián)素、瘦素及胰島素抵抗水平,監(jiān)測(cè)大鼠脂肪組織AMPK、葡萄糖轉(zhuǎn)運(yùn)蛋白(GLUT4)水平,并進(jìn)行統(tǒng)計(jì)學(xué)分析。結(jié)果間歇缺氧大鼠總膽固醇、三酰甘油、腫瘤壞死因子-α(TNF-α)、白細(xì)胞介素(IL)-6、IL-2、核因子κB(NF-κB)、缺氧誘導(dǎo)因子(HIF-1)顯著高于對(duì)照組(P0.05);脂聯(lián)素、瘦素及胰島素抵抗指數(shù)顯著低于對(duì)照組(P0.05)。使用AMPK激活劑后的大鼠體內(nèi)炎癥因子釋放減少,脂聯(lián)素、瘦素含量增加,血脂、胰島素抵抗情況較前有改善,GLUT4水平增加。而使用AMPK抑制劑處理后大鼠體內(nèi)炎癥因子、脂聯(lián)素、瘦素水平均上升,胰島素抵抗更嚴(yán)重,GLUT4水平也進(jìn)一步下降。結(jié)論 AMPK能夠減少炎癥介質(zhì)的釋放,促進(jìn)脂聯(lián)素、瘦素的釋放,增加GLUT4水平,改善胰島素抵抗,從而調(diào)節(jié)能量代謝及炎癥介質(zhì),為臨床治療OSAS相關(guān)疾病提供新的思路與靶點(diǎn)。
[Abstract]:Objective to investigate the effect and mechanism of adenosine monophosphate activated protein kinase (AMPK) activation on insulin resistance and inflammatory factors in rats with chronic intermittent hypoxia. Methods 36 male SD rats were divided into normoxic control group, 2-week intermittent hypoxia group and 8-week intermittent hypoxia group. The model of chronic intermittent hypoxia rat model was established to simulate obstructive sleep apnea syndrome. 36 male SD rats were divided into normoxic control group, 2-week intermittent hypoxia group and 8-week intermittent hypoxia group. The levels of inflammatory mediators, blood lipids, adiponectin, leptin and insulin resistance in rats treated with AMPK agonists and AMPK inhibitors were observed. The levels of AMPK, glucose transporter (GLUT4) in adipose tissue of rats were monitored and statistically analyzed. Results the total cholesterol, triacylglycerol, tumor necrosis factor-偽 (TNF- 偽), IL-6, IL 鈮，

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