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作 者:邓满香[1] 刘慧霞[2] 张骥[2] 杨幼波[2]
机构地区:[1]厦门大学附属中山医院老年科,福建省厦门361004 [2]中南大学湘雅医院老年病科
出 处:《中国医师杂志》2012年第12期1606-1608,共3页Journal of Chinese Physician
摘 要:目的探讨纤溶酶原激活物抑制剂-1(PAI-1)及肿瘤坏死因子-α(TNF—α)与代谢综合征(Metabolic syndrome,MS)及并发冠心病发病的关系,并探讨二甲双胍对PAI-1、TNF-α及MS的影响。方法老年MS患者60例,分成两组各30例:二甲双胍组予生活方式及二甲双胍干预治疗,生活干预组仅予生活方式干预。另选择同期健康体检者30例为对照组,发色底物法检测血浆PAI-1水平,ELISA法检测TNF-α水平。结果(1)老年MS患者血PAI-1活性、TNF-α水平[(0.95±0.05)AU/ml、(24.81±3.87)ng/ml]明显高于对照组[(0.66±0.10)AU/ml、(10.76±2.00)ng/ml](P〈0.001);(2)Ms组合并CHD者血PAI-1活性、TNF—α水平[(0.96±0.05)AU/ml、(26.12±2.83)ng/m1]明显高于未合并CHD者[(0.94±0.03)AU/ml、(23.71±4.27)ng/ml](P〈0.05);(3)二甲双胍干预治疗能使PAI.1、TNF-α明显下降[△值分别为(0.20±0.17)AU/ml、(4.42±0.85ng/ml),P〈0.01],并能有效改善MS的多种成分。结论PAI-1、TNF-α参与老年MS及其并发症的发生,二甲双胍能降低这些患者的PAI-1及TNF—α水平,控制代谢综合征的各成分。Objective To explore the correlation of PAI-1 and TNF-α and the pathophysiology of the metabolic syndrome (MS) and coronary heart disease, and explore the role of mefformin in the MS. Methods Sixty eases of old patients with the MS were chosen. These patients were divided into two groups at random. One group interfered with living style and mefformin, the other group only interfered with living style. The activity of PAI-1 was detected by ehromogenic substrate method, and the level of TNF-α was detected by ELISA assay. Results (1) The levels of PAI-1 and TNF-α in the MS patients [ (0. 95 ± 0. 05) AU/ml, (24. 81± 3.87) ng/ml] were significantly higher than in normal old people[ (0. 66 ± 0. 10) AU/ ml, ( 10.76 ± 2.00) ng/ml ] ( P 〈 0. 001 ) ; (2)The levels of PAI-1 and TNF-α in the MS patients with CHD [ ( 0. 96 ± 0. 05 ) AU/ml, (26. 12 ± 2. 83 ) ng,/ml ] were significantly higher than those in the patients without CHD [ (0.94 ± 0. 03 )AU/ml, (23.71 ± 4. 27)ng/ml ] ( P 〈 0. 05 ) ;(3)The activity of PAI-1 and the level of TNF-ot in the mefformin group was decreased significantly [ A was ( 0. 20 ± 0. 17) AU/ml, (4. 42 ± 0. 85 ng/ml), P 〈 0.01 ], and metformin can improve the components of the MS. Conclusions The old patients with MS is prone to develop cardiac vascular disease. PAI-1 and TNF-α participate in pathophysiology of the MS and its complication. Metformin can inhibit the expression of PAI-1 and TNF-α to suppress the compo- nents of the MS, and block the complication of the MS.
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