期刊文献+

组织激肽释放酶与缺血性脑卒中患者预后的相关性研究

Correlative Exploration Between Tissue Kallikrein and the Prognosis of Cerebral Ischemic Stroke
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摘要 目的:探讨组织激肽释放酶(TK)与缺血性脑卒中(CIS)患者短期预后的关系。方法:采用酶联免疫吸附法检测280例CIS患者(试验组)和50例体检健康者(对照组)血浆TK,并对CIS患者进行神经功能缺损程度评分和牛津残障评分,探讨TK与其相关性。结果:①CIS患者急性期和恢复期血浆TK分别为(0.171±0.031)mg/L和(0.193±0.036)mg/L,均低于对照组(0.251±0.043)mg/L,差异有统计学意义(P<0.05);②CIS患者急性期神经功能缺损评分(22.86±3.21)显著高于恢复期(13.12±1.45),差异有统计学意义(P<0.05);③CIS患者急性期和恢复期血浆TK水平与神经功能缺损评分均显著负相关(r分别为-0.582和-0.473,均P<0.05);④预后良好组急性期和恢复期血浆TK水平分别为(0.176±0.036)、(0.198±0.040)mg/L,均相应高于对照组急性期(0.159±0.023)和恢复期(0.184±0.027)mg/L,差异均有统计学意义(P<0.05)。结论:TK水平下降预示CIS患者预后不良。 Objective To explore correlativity between tissue kallikreir, (TK) and the prognosis of cerebral ischemic stroke (CIS). Methods The concentration of plasma TK was measured in 280 CIS patients, as well as in 60 normal healthy persens as con- trois. The function defect score and the oxford handicap scale were evalvated in the CIS patients, too. Correlative analysis was used to realize the relationship between TK and the function defect score. Results The concentration of TK in the acute stage and recovery stage in the CIS patients was (0.171± 0.031 )mg/L and (0. 193 ± 0.036 )mg/L respectively, and showed significantly lower than that in the control group(0.251 ±0.043) ; The function defect score in the acute stage expressed significantly higher than that of recovery stage in CIS patients(P 〈0.05) ; The TK proved significantly negative correlated with the function defect score beth in the acute stage and recovery stage(P 〈0.05). The concentration of TK indicated significantly lower in the poor prognosis group than that in the good prognosis group both in the acute stage and recovery stage (P 〈 0.05). Conclusion The lower concentration of TK predict poor prog- nosis in the CIS patients.
出处 《放射免疫学杂志》 CAS 2013年第5期618-620,共3页 Journal of Radioimmanology
关键词 组织激肽释放酶 缺血性脑卒中 预后 tissue kallikrein, cerebral ischemic stroke, prognosis
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  • 1Wang YD, Lu RY, Huang XX, et al. Human tissue kallikrein promoted activation of the ipsilesional sensorimotor cortex after acute cere- bral infarction[J]. Eur Neural, 2011, 65(4): 208-214.
  • 2Liu L,Zhang R, Liu K, et al. Tissue kallikrein alleviates gluta- mate-induced neumtoxicity by activating ERK1 [ J ]. J Neurosci Res, 2009, 87(16) : 3576-3590.
  • 3Zhang Q, Ding H, Yan J, et al. Plasma tissue kallikrein level is negatively associated with incident and recurrent stroke: a multieenter ease-control study in China[J]. Ann Neurol, 2011,70(2) : 265-273.
  • 4章永强,袁芬芬,应小卫,王希佳.血尿酸和胆红素及血脂水平与缺血性脑卒中的相关关系研究[J].中国全科医学,2011,14(11):1178-1180. 被引量:25
  • 5许贵刚,朱在卿,刘洋,郭艳丽.缺血性脑卒中患者血浆氧化低密度脂蛋白与预后的相关性研究[J].中国全科医学,2011,14(17):1882-1883. 被引量:15
  • 6刘平,丁爱华,周小毛.颅脑损伤患者早期凝血功能与颅脑损伤程度和预后的关系[J].中国现代医生,2009,47(16):23-24. 被引量:12
  • 7Liu L, Zhang R, Liu K, et al. Tissue kallikrein protects cortical neurons against in vitro ischemia-acidosis/roperfusion-induced injury through the ERK1/2 pathway [ J ]. Exp Neural, 2009, 219 ( 2 ) : 453-465.
  • 8Xia CF, Yin H, Borlongan CV, et al. Kanikrein gene transfer pro- tects against isehemic stroke by promoting glial cell migration and inhibi- ting apoptosis[ J]. Hypertension, 2004, 43 (2) : 452-159.
  • 9Xia CF, Yin H, Yao YY, et al. Kallikrein protects against ische- mic stroke by inhibiting apoptosis and inflammation and promoting angio- genesis and neurogenesis [ J ]. Hum Gene Ther, 2006, 17 ( 2 ) : 206-219.

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