中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2012年
12期
1606-1608
,共3页
邓满香%刘慧霞%张骥%杨幼波
鄧滿香%劉慧霞%張驥%楊幼波
산만향%류혜하%장기%양유파
纤溶酶原激活物抑制物1/血液%肿瘤坏死因子α/血液%代谢综合征X/血液%二甲双胍/治疗应用胍
纖溶酶原激活物抑製物1/血液%腫瘤壞死因子α/血液%代謝綜閤徵X/血液%二甲雙胍/治療應用胍
섬용매원격활물억제물1/혈액%종류배사인자α/혈액%대사종합정X/혈액%이갑쌍고/치료응용고
Plasminogen activator inhibitor 1/blood%Tumor necrosis factor-alpha/blood%Metabolic syndrome X/blood%Metformin/therapeutic use
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、(1O.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/ml]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±0.85 ng/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.
目的 探討纖溶酶原激活物抑製劑-1(PAI-1)及腫瘤壞死因子-α(TNF-α)與代謝綜閤徵(Metabolic syndrome,MS)及併髮冠心病髮病的關繫,併探討二甲雙胍對PAI-1、TNF-α及MS的影響.方法 老年MS患者60例,分成兩組各30例:二甲雙胍組予生活方式及二甲雙胍榦預治療,生活榦預組僅予生活方式榦預.另選擇同期健康體檢者30例為對照組,髮色底物法檢測血漿PAI-1水平,ELISA法檢測TNF-α水平.結果 (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]明顯高于對照組[(0.66 ±0.10) AU/ml、(1O.76±2.00) ng/ml](P＜0.001)；(2)MS組閤併CHD者血PAI-1活性、TNF-α水平[(0.96±0.05) AU/ml、(26.12±2.83) ng/ml]明顯高于未閤併CHD者[(0.94 ±0.03) AU/ml、(23.71±4.27)ng/ml](P＜0.05)；(3)二甲雙胍榦預治療能使PAI-1、TNF-α明顯下降[△值分彆為(0.20 ±0.17) AU/ml、(4.42±0.85 ng/ml),P＜0.01],併能有效改善MS的多種成分.結論 PAI-1、TNF-α參與老年MS及其併髮癥的髮生,二甲雙胍能降低這些患者的PAI-1及TNF-α水平,控製代謝綜閤徵的各成分.
목적 탐토섬용매원격활물억제제-1(PAI-1)급종류배사인자-α(TNF-α)여대사종합정(Metabolic syndrome,MS)급병발관심병발병적관계,병탐토이갑쌍고대PAI-1、TNF-α급MS적영향.방법 노년MS환자60례,분성량조각30례:이갑쌍고조여생활방식급이갑쌍고간예치료,생활간예조부여생활방식간예.령선택동기건강체검자30례위대조조,발색저물법검측혈장PAI-1수평,ELISA법검측TNF-α수평.결과 (1)노년MS환자혈PAI-1활성、TNF-α수평[(0.95±0.05)AU/ml、(24.81 ±3.87) ng/ml]명현고우대조조[(0.66 ±0.10) AU/ml、(1O.76±2.00) ng/ml](P＜0.001)；(2)MS조합병CHD자혈PAI-1활성、TNF-α수평[(0.96±0.05) AU/ml、(26.12±2.83) ng/ml]명현고우미합병CHD자[(0.94 ±0.03) AU/ml、(23.71±4.27)ng/ml](P＜0.05)；(3)이갑쌍고간예치료능사PAI-1、TNF-α명현하강[△치분별위(0.20 ±0.17) AU/ml、(4.42±0.85 ng/ml),P＜0.01],병능유효개선MS적다충성분.결론 PAI-1、TNF-α삼여노년MS급기병발증적발생,이갑쌍고능강저저사환자적PAI-1급TNF-α수평,공제대사종합정적각성분.
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 metformin in the MS.Methods Sixty cases of old patients with the MS were chosen.These patients were divided into two groups at random.One group interfered with living style and metformin,the other group only interfered with living style.The activity of PAI-1 was detected by chromogenic 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-α in the metformin group was decreased significantly [△ was (0.20 ± 0.17)AU/ml,(4.42 ± 0.85ng/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 components of the MS,and block the complication of the MS.
