急性脑梗死患者高迁移率族蛋白B1和过氧化小体增殖剂激活型受体γmRNA的表达

被引:2
作者
张一娜 [1 ]
王莉 [1 ]
刘向娟 [1 ]
俞春江 [2 ]
程露杨 [1 ]
机构
[1] 哈尔滨医科大学附属第二医院老年病科
[2] 哈尔滨医科大学附属第二医院
关键词
脑梗死; 高迁移率族蛋白质类; 过氧化小体增殖剂激活型受体;
D O I
暂无
中图分类号
R743.33 [脑栓塞];
学科分类号
摘要
目的研究急性脑梗死患者血清高迁移率族蛋白B1(HMGBl)与外周血淋巴细胞过氧化小体增殖剂激活型受体γ(PPARγ)mRNA表达的变化,及二者与脑梗死体积的相关性。方法连续收集2010年7月—12月哈尔滨医科大学附属第二医院老年病科及神经内科就诊的发病3 d以内的急性脑梗死患者72例及对照人群70例。用ELISA法测定两组患者血清中HMGB1,用实时RT-PCR法测定两组患者空腹周围血淋巴细胞PPARγmRNA的表达情况。根据脑梗死患者发病后48~72 h CT检查结果,计算脑梗死体积。结果①梗死组患者PPA脚mRNA表达水平(0.54±0.37)低于对照组(1.98±0.35),血清HMGBl水平(12.7±6.1)μg/L高于对照组(2.2±0.8)μg/L,差异有统计学意义,P<0.01。②脑梗死患者周围血淋巴细胞PPA脚mRNA表达水平与血清HMGBl水平呈负相关,r=-0.843,P<0.01。③经相关性分析,脑梗死患者PPARγmRNA表达水平与脑梗死体积呈负相关,r=-0.886,P<0.01;脑梗死患者HMGB1水平和脑梗死体积呈正相关,r=0.847,P<0.01。结论在脑梗死急性期,PPARγ和HMGB1均参与脑缺血炎性反应,HMGB1及PPARγ脚mRNA表达水平可反映急性脑梗死患者梗死体积的大小。
引用
收藏
页码:342 / 346
页数:5
相关论文
共 10 条
[1]   晚期炎症介质HMGB1的病理生理作用 [J].
唐道林 ;
康睿 ;
肖献忠 .
中国病理生理杂志, 2005, (07) :1426-1430
[2]   脑梗死患者PPARγmRNA表达变化和脑梗死体积关系的研究 [J].
刘运海 ;
刘尊敬 ;
杨期东 ;
张宁 .
卒中与神经疾病, 2004, (02) :71-73
[4]   Cerebroprotective action of telmisartan by inhibition of macrophages/microglia expressing HMGB1 via a peroxisome proliferator-activated receptor γ-dependent mechanism [J].
Haraguchi, Tamami ;
Takasaki, Kotaro ;
Naito, Tetsuya ;
Hayakawa, Kazuhide ;
Katsurabayashi, Shutaro ;
Mishima, Kenichi ;
Iwasaki, Katsunori ;
Fujiwara, Michihiro .
NEUROSCIENCE LETTERS, 2009, 464 (03) :151-155
[5]  
Delayed Treatment With Minocycline Ameliorates Neurologic Impairment Through Activated Microglia Expressing a High-Mobility Group Box1–Inhibiting Mechanism[J] . Kazuhide Hayakawa,Kenichi Mishima,Masanori Nozako,Mai Hazekawa,Shohei Mishima,Masayuki Fujioka,Kensuke Orito,Nobuaki Egashira,Katsunori Iwasaki,Michihiro Fujiwara.Stroke . 2008 (3)
[6]   HMGB1 expression by activated vascular smooth muscle cells in advanced human atherosclerosis plaques [J].
Inoue, Katsumi ;
Kawahara, Ko-ichi ;
Biswas, Karnal Krishna ;
Ando, Kenji ;
Mitsudo, Kazuaki ;
Nobuyoshi, Masakiyo ;
Maruyama, Ikuro .
CARDIOVASCULAR PATHOLOGY, 2007, 16 (03) :136-143
[7]   High-mobility group box 1 activates integrin-dependent homing of endothelial progenitor cells [J].
Chavakis, Emmanouil ;
Hain, Andreas ;
Vinci, Maria ;
Carmona, Guillaume ;
Bianchi, Marco E. ;
Vajkoczy, Peter ;
Zeiher, Andreas M. ;
Chavakis, Triantafyllos ;
Dimmeler, Stefanie .
CIRCULATION RESEARCH, 2007, 100 (02) :204-212
[8]   Peroxisome proliferator-activated receptor gamma activation decreases neuroinflammation in brain after stress in rats [J].
García-Bueno, B ;
Madrigal, JLM ;
Lizasoain, I ;
Moro, MA ;
Lorenzo, P ;
Leza, JC .
BIOLOGICAL PSYCHIATRY, 2005, 57 (08) :885-894
[9]   Endogenous PPARγ mediates anti-inflammatory activity in murine ischemia-reperfusion injury [J].
Nakajima, A ;
Wada, K ;
Miki, H ;
Kubota, N ;
Nakajima, N ;
Terauchi, Y ;
Ohnishi, S ;
Saubermann, LJ ;
Kadowaki, T ;
Blumberg, RS ;
Nagai, R ;
Matsuhashi, N .
GASTROENTEROLOGY, 2001, 120 (02) :460-469
[10]   SMALL DEEP INFARCTS DIAGNOSED ON COMPUTED-TOMOGRAPHY [J].
PULLICINO, P ;
NELSON, RF ;
KENDALL, BE ;
MARSHALL, J .
NEUROLOGY, 1980, 30 (10) :1090-1096