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脑梗死患者PPARγmRNA表达变化和脑梗死体积关系的研究 被引量:10

Expressoin of PPARγ mRNA in patients with acute cerebral infarction and its relationship with infarct volume
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摘要 目的 探讨脑梗死患者PPARγmRNA表达变化和脑梗死体积的关系。方法 序贯收集2002年7月~2003年1月在湘雅医院神经内科就诊的发病3天以内的符合入选标准的脑梗死患者32例,同时收集相匹配的同期体检者30例作对照。用RT-PCR法测定两组对象空腹周围血淋巴细胞PPARγmRNA表达情况。所有脑梗死患者依据发病后48~72小时CT检查结果,计算脑梗死体积。结果 脑梗死患者和对照组PPARγmRNA表达值分别为0.238±0.05和0.841±0.07,两组比较差异显著;脑梗死患者PPARγmRNA表达和脑梗死体积呈负相关(r=-0.664,P<0.001)。结论 发病3天内脑梗死患者周围血淋巴细胞PPARγmRNA表达下调,并和脑梗死体积呈负相关。 Objective To study the expression of PPARγ mRNA in patients with acute cerebral infarct and the relationship between PPARγ mRNA and infarct volume. Methods Thirty two patients at Xiangya Hospital experienced cerebral infarcts that occurred within the first 3 days were consecutively incorporated into the study between July 2002 and January 2003, and 30 healthy subjects were selected as control group. The expression of the PPARy mRNA in the lymphocyte located in peripheral blood was detected by RT-PCR. The subsequent volume of brain lesion as a consequence of stroke were measured by CT within 48-72 hours after the onset. Results The patients displayed decreased expression of PPARy mRNA within the first three days after stroke onset compared with the control subjects (P<0.001). The infarct volume was in negative correlation with the expression of PPARy mRNA (r = - 0.664, P < 0.001). Conclusions The expression of PPARy mRNA decreased in patients with cerebral infarct in the first three days and displayed a neglative correlation with infarct volume.
出处 《卒中与神经疾病》 2004年第2期71-73,共3页 Stroke and Nervous Diseases
关键词 脑梗死 PPARΓ MRNA 脑梗死体积 RT-PCR法 淋巴细胞 PCR电泳凝胶图 Cerebral infarcts Peroxisome prolifterator-activated receptor gamma Infarction volume
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  • 1Yue TL, Chen J, Bao W, et al. In vivo myocardial protection from ischemia/reperfu,sion injury by the peroximme proliferator-activated receptor-ganmla agonist rosiglitazone. Circulation, 2001, 104 (21) :2588-2594.
  • 2Shiomi T, Tsmsui H, Hayashidani S, et al. Pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist,attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation, 2002,106 (24) : 3126-3132.
  • 3Okada M, Yan SF, Pinsky DJ. Peroxisome proliferator-activated receptor-gamma( PPAR-gamma ) activation suppre.,kses ischemic induction of Egr-1 and its inflammatory gene targets. FASEB J,2002, 16(14) : 1861-1868.
  • 4Pullicino P. Small deed infarcts diagnosed on computed tomograph. Nearology, 1980,30(10) : 1890-1896.
  • 5Atsushi N, Koichiro W, Hiroshi M, et al. Endogenous PPARgarnma mediates anti inflammatory activity in murine ischemia-reperfusion iniury. Gastroenterology, 2001,120 (2) : 460-469.
  • 6Khandoudi N, Delerive P, Berrebi-Bertrand I, et al. Rosiglitazone, a peroxisome proliferator-activated receptor-gamma, inhibits the Jun NH(2)-terminal kinase/activating protein 1 pathway and protects the heart from ischemia/reperfusion injury. Diabetes, 2002,51 ( 5 ) :1507-1514.
  • 7Wayman NS, Hattori Y, McDonald, et al. Ligands of the peroxisome proliferator-activated receptors(PPAR-gamma and PPAR-alpha) reduce myocardial infarct size. FASEB J, 2002,16(9) : 1027-1040.

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