本文關鍵詞： 高尿酸血癥 糖尿病 解偶聯(lián)蛋白 氧化應激 心肌細胞　出處：《解放軍醫(yī)學雜志》2017年06期 　論文類型：期刊論文

【摘要】：目的研究解偶聯(lián)蛋白2(UCP2)在高糖高脂高尿酸小鼠心肌細胞(MCM)中的作用及機制。方法以25mmol/L高糖培養(yǎng)基+300μmol/L軟脂酸鈉干預MCM 18h模擬合并高脂血癥的2型糖尿病組(高糖+高脂組),在糖尿病組的基礎上再用1500μmol/L尿酸干預18h模擬2型糖尿病合并高尿酸組(高糖+高脂+高尿酸組)。隨后,采用UCP2抑制劑Genipin抑制心肌線粒體UCP2表達,進一步將2型糖尿病合并高尿酸組分為溶媒對照組、Genipin組。研究UCP2在高糖高脂合并高尿酸心肌細胞損傷的機制時,再分為Genipin組、Genipin+N-乙酰半胱氨酸(NAC)組。采用流式細胞儀檢測各組心肌細胞的凋亡水平,q-PCR法和Western blotting檢測心肌細胞中UCP2的表達情況,DHE染色及ELISA法檢測活性氧簇(ROS)水平。結果與高糖+高脂組比較,高糖+高脂+高尿酸組心肌細胞凋亡明顯增加(P0.05),心肌細胞中UCP2的表達水平明顯降低,同時ROS的水平明顯上升(P0.05)。采用Genipin抑制UCP2的表達水平后,高糖高脂高尿酸干預后心肌細胞凋亡水平及ROS水平升高更加明顯(P0.05)。在此基礎上應用抗氧化劑NAC后,高尿酸所誘導的心肌細胞凋亡及ROS升高被明顯逆轉(P0.05)。結論 UCP2可以通過抑制氧化應激緩解高糖高脂合并高尿酸所誘導的心肌細胞凋亡。
[Abstract]:Objective to study the role and mechanism of uncoupling protein 2 (UCP2) in cardiac myocytes of mice with high glucose, high lipid and high uric acid. Methods the MCM 18 h model of type 2 diabetes mellitus with hyperlipidemia (hyperglycemia) was induced by intervention of 300渭 mol/L sodium palmitate on 25mmol / L high glucose medium. Hyperlipidemia group was treated with 1 500 渭 mol/L uric acid for 18 h to simulate type 2 diabetes mellitus with high uric acid (high glucose, high fat and high uric acid group). Genipin, a UCP2 inhibitor, was used to inhibit the expression of mitochondrial UCP2 in myocardium. Type 2 diabetes mellitus with hyperuricemia was further divided into two groups: control group. The mechanism of hyperglycemia and hyperuricemia induced by UCP2 was studied. The apoptosis level of cardiac myocytes was detected by flow cytometry and the expression of UCP2 in cardiac myocytes was detected by Western blotting. The level of reactive oxygen species (Ros) was detected by ELISA method. Results compared with high glucose and high fat group, In high glucose, high lipid and high uric acid groups, the apoptosis of cardiac myocytes increased significantly, while the expression of UCP2 in cardiac myocytes decreased, while the level of ROS increased significantly. Genipin inhibited the expression of UCP2. After intervention with high glucose, high fat and high uric acid, the levels of cardiomyocyte apoptosis and ROS increased more obviously. On this basis, the antioxidant NAC was applied. The apoptosis of cardiomyocytes induced by high uric acid and the increase of ROS were obviously reversed by P0.05.Conclusion UCP2 can alleviate the apoptosis induced by high glucose and high lipid combined with high uric acid by inhibiting oxidative stress.
【作者單位】： 西南醫(yī)科大學臨床醫(yī)學院;成都軍區(qū)總醫(yī)院心血管內科;
【基金】：國家自然科學基金(81500208) 四川省科技廳杰出青年基金(2017JQ0012) 四川省科技支持計劃項目(2015JY0277) 博士后醫(yī)院管理基金(41732BA)~~
【分類號】：R587.2

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