期刊文献+

CD36促进脑出血患者血肿吸收及其临床意义 被引量:5

CD36 promotes hematoma absorption in patients with intracerebral hemorrhage and its clinical significance
下载PDF
导出
摘要 目的探讨CD36对脑出血患者血肿吸收及神经功能缺损的影响。方法选择2012年7月至2014年6月在第三军医大学新桥医院神经内科住院治疗的349例脑出血患者为研究对象,获得患者静脉全血后进行CD36突变筛查,在突变的35例患者中挑选出24例为基底节区出血的患者分入CD36缺陷组,同时在CD36正常的患者中挑选出24例基线水平一致的基底节区出血患者(CD36正常组),比较2组患者的血肿吸收、炎症变化及神经功能缺损评分。结果 349例脑出血患者中筛选出35例CD36缺陷患者(10.03%)。2组患者的年龄、性别、入院时血肿体积、危险因素等基线水平差异无显著性(P>0.05)。发病7 d后CD36缺陷患者血肿吸收速率低于CD36正常患者[(22.4±2.4)%vs(44.8±5.1)%,P<0.05],并且CD36缺陷患者炎症因子下降较CD36正常患者慢(P<0.05)。神经功能缺损评分显示CD36缺陷患者在第14、30、90天时显著高于CD36正常患者(P<0.05)。结论CD36可能在促进血肿吸收中具有重要作用进而影响患者的神经功能恢复。 Objective To investigate the influence of CD36 in hematoma absorption and neurologic deficit scores( NDS) in the patients with intracerebral hemorrhage( ICH). Methods A total of 349 ICH patients treated in our department from July 2012 to June 2014 were selected as the research objects. Among them,24 ICH patients with cerebral basilar hemorrhage were selected from 35 patients with CD36 mutation,and divided into CD36-deficiency group. Meanwhile,24 CD36-normal ICH patients who had similar features with the CD36-deficency group were selected as the CD36-normal group. The hematoma absorption,inflammatory responses and NDS of the 2 groups were compared. Results Thirty-five patients( 10. 03%)with CD36 deficiency were screened from the 349 ICH patients. There were no significant differences in the age,gender,hematoma volume on admission,risk factors,and other baseline data between the 2 groups( P〉0. 05). On day 7 after ICH,the hematoma absorption of CD36-deficiency patients was significantly lower than that of CD36-normal patients( 22. 4% ± 2. 4% vs 44. 8% ± 5. 1%,P〈0. 05),as well as the reduction rate of pro-inflammatory factors on day 14 after ICH( P〈0. 05). Moreover,on the days 14,30 and 90 after ICH,the NDS of CD36-deficiency patients were higher than those of CD36-normal patients( P〈0. 05).Conclusion CD36 may play an important role in promoting the hematoma absorption and improving the NDS after ICH.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2015年第8期792-796,共5页 Journal of Third Military Medical University
基金 国家自然科学基金面上项目(81271283) 国家重点基础研究发展计划(973计划 2014CB541605)~~
关键词 脑出血 血肿吸收 炎症 CD36 神经功能缺损评分 intracerebral hemorrhage hematoma absorption inflammation CD36 neurologic deficit scores
  • 相关文献

参考文献17

  • 1Keep R F, Hua Y, Xi G. Intracerebral haemorrhage: mecha- nisms of injury and therapeutic targets [ J ]. Lancet Neurol, 2012, 11(8) : 720 -731.
  • 2罗丹,李芳芳,王啸,陈亮,谢鹏.自发性脑出血患者并发症的相关危险因素分析[J].第三军医大学学报,2012,34(14):1438-1441. 被引量:14
  • 3朱孔江,徐广振,杨辉.小鼠脑出血模型血肿周围雌激素受体的表达[J].第三军医大学学报,2013,35(17):1877-1879. 被引量:1
  • 4Zhou Y, Wang Y, Wang J, et al. Inflammation in intracere- bral hemorrhage: from mechanisms to clinical translation [ J ]. Prog Neurobiol, 2014, 115:25-44.
  • 5Mendelow A D, Gregson B A, Rowan E N, et al. Early sur- gery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH Ⅱ ) : a randomised trial [ J ]. Lancet, 2013, 382 (9890) : 397 - 408.
  • 6Silverstein R L, Febbraio M. CD36, a scavenger receptor in- volved in immunity, metabolism, angiogenesis, and behavior [ J]. Sci Signal, 2009, 2 (72) : re3.
  • 7Silverstein R L. Inflammation, atherosclerosis, and arterial thrombosis : role of the scavenger receptor CD36 [ J ]. Cleve Clin J Med, 2009, 76 Suppl 2 : S27 - S30.
  • 8Zhao X, Sun G, Zhang J, et al. Hematoma resolution as a target for intracerebral hemorrhage treatment: role for peroxi- some proliferator-activated receptor gamma in microglia/mac- rophages[J]. Ann Neurol, 2007, 61(4): 352-362.
  • 9Sansing L H, Harris T H, Welsh F A, et al. Toll-like recep- tor 4 contributes to poor outcome after intracerebral hemor- rhage[J]. Ann Neurol, 2011,70(4) : 646 -656.
  • 10Fang H, Chen J, Lin S, et al. CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regu- lation by TLR4 signaling[J]. J Immunol, 2014, 192(12) : 5984 - 5992.

二级参考文献46

  • 1秦平,侯明,石艳,孙建芝,朱媛媛,李丽珍,彭军,张茂宏.慢性ITP患者血小板膜表面GPⅣ、GPⅤ特异性自身抗体的测定[J].中国免疫学杂志,2005,21(2):139-141. 被引量:1
  • 2Ohto H,Miura S,Ariga H,李执如,周琼秀.胎儿血小板抗原引起母亲免疫反应的回顾调查[J].国外医学(输血及血液学分册),2005,28(6):561-564. 被引量:4
  • 3林小荣,林春暖,许月明,钟娉红,黄彩华,潘素琪.急性脑卒中并肺部感染临床分析[J].临床和实验医学杂志,2006,5(6):654-655. 被引量:9
  • 4魏莉萍,黄晓哲.预防和控制神经内科重症监护病房患者肺部感染的护理体会[J].中国实用神经疾病杂志,2007,10(6). 被引量:6
  • 5盖全武 李莉 田扬 等.急性脑出血并发多脏器功能衰竭68例临床探讨.中国医药指南,2005,3(6):631-632.
  • 6Ogata T. CD36 (Naka) sensitiztion with platelet-transfusiort re- fractoriness in a liver transplant recipient. Transplarttation, 2005, 79(5) :620.
  • 7Fujino H, Ohta K,Taniue J, et al. Primary refractoriness to platelet transfusion caused by Nak (a) antibody alone. Vox Sang, 2001,81 (1) :42-44.
  • 8Rock G, Clark W, Stembach M, et al. Haemolytic uraemic syn- drome is an immune-mediated disease:role of artti-CD36 antibod- ies. Br J Haematol,2005,131 (2) :247-252.
  • 9Morishita K, Wakamoto S,Miyazaki T,et al. Life-threatening ad- verse reaction followed by thrembocytopenia after passive transfu- sion of fresh frozen plasma. Transfusion,2005,45 (5) :803-806.
  • 10Wakamoto S, Fujihara M, Urushibara N, et al. Heterogeneity of platelet responsivness to anti-CD36 in plasma associated with ad- verse transfusion reactions. Vox Sang,2005,88( 1 ) .41-51.

共引文献30

同被引文献74

  • 1东贵荣,吴宝柱,张宣.百会、太阳穴配伍治疗急性脑出血的临床研究[J].中医杂志,1994,35(5):276-277. 被引量:29
  • 2陈万群,骆婕,彭锐锐,吴颜晖,莫宏波,冯烈,李菊香,刘誉.SR-AⅡ和CD36的表达水平与AGEs及糖尿病并发症的相关性研究[J].中国病理生理杂志,2007,23(1):168-172. 被引量:15
  • 3MayerSA, RinconF. Treatment of intracerebral haemorrhage[J]. Lancet Neurol, 2005, 4(10): 662-672. DOI: 10.1016/S1474-4422(05)70195-2.
  • 4EgashiraY, HuaY, KeepRF, et al. Intercellular cross-talk in intracerebral hemorrhage[J]. Brain Res, 2015, 1623: 97-109. DOI: 10.1016/j.brainres.2015.04.003.
  • 5ZoeteV, GrosdidierA, MichielinO. Peroxisome proliferator-activated receptor structures: ligand specificity, molecular switch and interactions with regulators[J]. Biochim Biophys Acta, 2007, 1771(8): 915-925. DOI: 10.1016/j.bbalip.2007.01.007.
  • 6SchuppM, LazarMA. Endogenous ligands for nuclear receptors: digging deeper[J]. J Biol Chem, 2010, 285(52): 40409-40415. DOI: 10.1074/jbc.R110.182451.
  • 7LehmannJM, MooreLB, Smith-OliverTA, et al. An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor γ (PPAR γ)[J]. J Biol Chem, 1995, 270(22): 12953-12956. DOI: 10.1074/jbc.270.22.12953.
  • 8SunL, XuYW, HanJ, et al. 12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ:a possible neuroprotective effect in ischemic brain[J]. J Lipid Res, 2015, 56(3): 502-514. DOI: 10.1194/jlr.M053058.
  • 9M?kel?J, TselykhTV, KukkonenJP, et al. Peroxisome proliferator-activated receptor-γ (PPARγ) agonist is neuroprotective and stimulates PGC-1α expression and CREB phosphorylation in human dopaminergic neurons[J]. Neuropharmacology, 2016, 102: 266-275. DOI: 10.1016/j.neuropharm.2015.11.020.
  • 10WuG, WuJ, JiaoY, et al. Rosiglitazone infusion therapy following minimally invasive surgery for intracerebral hemorrhage evacuation decreases matrix metalloproteinase-9 and blood-brain barrier disruption in rabbits[J]. BMC Neurol, 2015, 15: 37. DOI: 10.1186/s12883-015-0287-3.

引证文献5

二级引证文献9

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部