期刊文献+

腺苷A_(2a)受体激活对脑出血后炎症反应和细胞凋亡的影响 被引量:1

Effect of adenosine receptor A_(2a) activation on the inflammation and apoptosis after intracerebral hemorrhage
原文传递
导出
摘要 目的探讨脑出血(ICH)后激活腺苷A2A受体对中性粒细胞浸润、TNF-α蛋白的表达及细胞凋亡的影响。方法 SD大鼠随机分为对照组、ICH组、CGS组、CGS+ZM组、ZM组。应用胶原酶脑内立体定向注射制作ICH模型。对照组注射生理盐水2ul,CGS组、CGS+ZM组、ZM组在ICH模型制作前15min,脑内立体定向分别注射CGS1μg,CGS1μg+ZM1μg,ZM1μg。模型制作后24h处死动物,应用HE染色检测中性粒细胞的浸润,应用Western-Blot技术检测TNF-α蛋白的表达,应用TUNEL法检测细胞凋亡。结果 ICH组可见明显的中性粒细胞浸润、TNF-α蛋白的表达及凋亡的细胞,与对照组比较,差别具有显著性(P<0.001)。CGS组中性粒细胞浸润、TNF-α的表达及凋亡的细胞数目明显降低,与ICH组比较,差别具有显著性(P<0.001)。CGS+ZM组中性粒细胞浸润、TNF-α的表达及凋亡的细胞明显增高,与ICH组比较差异无显著性(P>0.05),与CGS组比较差异具有显著性(P<0.001)。结论选择性的腺苷A2a受体激活可降低ICH后的炎症反应和细胞凋亡,从而减轻ICH后组织的损伤。 Objective To investigate the effect of adenosine receptor A2a activation on the neurophil cellular infiltration,expression of TNF-α protein and apoptosis after intracerebral hemorrhage(ICH).Methods SD rats were randomly divided into control,ICH,CGS,CGS+ZM,and ZM groups.ICH models were performed by collagenase stereotaxical injection.Control group were injected 2 ul physiologic saline.CGS,CGS+ZM and ZM group were respectively injected CGS 1 μg,CGS 1 μg+ZM 1 μg and ZM 1 μg at 15 minutes before ICH models were performed.Rats were put to death at 24 th hour after modeling.Neurophil cellular infiltration was detected by HE dyeing.Expression of TNF-α protein was determined by Western-blot method.Apoptosis was measured by TUNEL method.Results Neurophil cellular infiltration,expression of TNF-α protein and apoptosis in ICH group were increased and had significant difference compared with control group(P〈0.001).Neurophil cellular infiltration,expression of TNF-α protein and apoptosis in CGS group were decreased and had significant difference compared with ICH group(P〈0.01).Neurophil cellular infiltration,expression of TNF-α protein and apoptosis in CGS+ZM group were incereased and had no significant difference compared with ICH group(P〉0.05).Conclusions Selective adenosine receptor A2a activation can depress inflammation and apoptosis after cerebral hemorrhage,and might reduce tissue injury in or surround hemotoma.
出处 《卒中与神经疾病》 2010年第4期195-198,201,共5页 Stroke and Nervous Diseases
关键词 脑出血 腺苷A2A受体 中性粒细胞 TNF-Α 细胞凋亡 Intracerebral hemorrhage Adenosine receptor A2a Neurophil cell TNF-α Apoptosis
  • 相关文献

参考文献13

  • 1Fredholm BB,Arslan G,Halldner L,et al.Adenosine receptor signaling in vitro and in vivo.Drug Dev Res,2001,52(4):274-282.
  • 2Fredholm BB,Chen JF,Cunha RA,et al.Adenosine and brain function.Int Rev Neurobiol.2005,63(3):191-270.
  • 3Xu K,Bastia E,Schwarzschild M.Therapeutic potential of adenosine A (2A) receptor antagonists in Parkinson's disease.Pharmacol Ther,2005,105(6):267-310.
  • 4Mayne M,Fotheringham J,Yan HJ,et a.Adenosine A2A receptor activation reduces proinflammatory events and decreases cell death following intracerebral hemorrhage.Ann Neurol,2001,49(6):727-735.
  • 5梁顺利,梅元武,邢宏义,方煌.实验性脑出血灶周MMP-9的表达与神经元凋亡的关系[J].卒中与神经疾病,2007,14(6):334-337. 被引量:2
  • 6Mayne M,Ni W,Yan HJ,et al.Antisense oligodeoxynucleotide inhibition of tumour necrosis factor-alpha expression is neuroprotective following intracerebral hemorrhage.Stroke,2001,32(4):240-248.
  • 7Pedata F,Gianfriddo M,Turchi D,et al.The protective effect of adenosine A2A receptor antagonism in cerebral ischemia.Neurol Res.2005,27(2):169-174.
  • 8Melani A,Gianfriddo M,Vannucchi MG,et al.The selective A2A receptor antagonist SCH 58261 protects from neurological deficit,brain damage and activation of p38 MAPK in rat focal cerebral ischemia.Brain Res,2006,16(1073-1074):470-480.
  • 9Nishizaki T.ATP2 and adenosine 2 mediated signaling in the central nervous system:adenosine stimulates glutamate release from astrocytes via A2a adenosine receptors.J Pharmacol Sci,2004,94(2):100-102.
  • 10Tebano MT,Martire A,Chiodi V,et al.Adenosine A2A receptors enable the synaptic effects of cannabinoid CB1 receptors in the rodent striatum.J Neurochem,2009,110(6):1921-1930.

二级参考文献11

  • 1Xue M,Del Bigio MR.Intracortical hemorrhage injury in rats:relationship between blood fractions and brain cell death.Stroke,2000,31 (7):1721-1727.
  • 2OpdenakkerG,Van den Steen PE,Dubois B,et al.Gelatinase B functions as regulator and effectorin leukocyte biology.J Leukoc Biol,2001,69(6):851-859.
  • 3Mayne M,Ni W,Yang HJ,et al.Antisense oligodeoxynucleotide inhibition of tumor necrosis factor-alpha expression is neuroprotective after intracerebral hemorrhage Stroke,2001,32 (1):240-248.
  • 4Power C,Henry S,Del Bigio MR,et al.Intracerebral hemorrhage induces macrophage activation and matrix metalloproteinases.Ann Neurol,2003,53 (6):731-742.
  • 5Hickenbottom SL,Grotta JC,Strong R,et al.Nuclear factor-κB and cell death after experimental intracerebral hemorrhage in rats.Stroke,1999,30(11):2472-2478.
  • 6Vaughan PJ,Pike CJ,Cotman CW,et al.Thrombin receptor activation protects neurons and astrocytes from cell death Produced by environmental insults.J Neurosci,1995,15 (7 Pt 2); 5389-5540.
  • 7Gu Z,Cui J,Brown S,et al.A highly specific inhibitor of matrix metalloproteinase-9 rescues laminin from proteolysis and neurons from apoptosis in transient focal cereb ral ischemia.J Neurosci,2005,25 (27):6401-6408.
  • 8张法永,陈衔城,任惠民,鲍伟民.缺血预处理对脑缺血血脑屏障通透性和MMP-9表达的影响[J].复旦学报(医学版),2001,28(3):216-219. 被引量:9
  • 9张毅,徐群,苏敏,苗玲,蔡琰.速避凝与丹参对缺血性脑卒中患者血浆中基质金属蛋白酶-9的影响[J].卒中与神经疾病,2003,10(5):274-276. 被引量:2
  • 10祝春华,董梅,张祥建.基质金属蛋白酶与神经系统疾病[J].脑与神经疾病杂志,2004,12(2):157-159. 被引量:1

共引文献1

同被引文献38

  • 1Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil ex- tracellular traps kill bacteria[ J]. Science, 2004, 303 (5663) : 1532-1535.
  • 2Chen JF, Eltzschig HK, Fredholm BB. Adenosine receptors as drug targets--what are the challenges? [J] Nat Rev Drug Discov, 2013, 12(4): 265-286.
  • 3Hasko G, Cronstein B. Regulation of inflammation by adenosine [J]. Front Immunol, 2013, 4: 85.
  • 4Eltzscbig HK, Sitkovsky MV, Robson SC. Purinergic signaling during inflammation[J]. N Engl J Med, 2012, 367(24) : 2322- 2333.
  • 5Poth JM, Brodsky K, Ehrentraut H, et al. Transcriptional con- trol of adenosine signaling by hypoxia-inducible transcription fac- tors during isehemic or inflammatory disease [ J ]. J Mol Med (Berl), 2013, 91(2): 183-193.
  • 6Ryzhov S, Solenkova NV, Goldstein AE, et al. Adenosine re- ceptor-mediated adhesion of endothelial progenitors to cardiac mi- crovascular endothelial cells [ J ]. Cire Res, 2008, 102 ( 3 ) : 356-363.
  • 7Lovatt D, Xu Q, Liu W, et al. Neuronal adenosine release, and not astrocytic ATP release, mediates feedback inhibition of excit- atory activity [ J ]. Proe Natl Acad Sei USA, 2012, 109 ( 16 ) : 6265 -6270.
  • 8Sullivan GW, Lee DD, Ross WG, et al. Activation of A2A a- denosine receptors inhibits expression of alpha 4/beta 1 integrin ( very late antigen-4 ) on stimulated human neutrophils [ J ]. J Leukoe Biol, 2004, 75( 1 ) : 127-134.
  • 9Glover DK, Riou LM, Ruiz M, et al. Reduction of infarct size and postischemic inflammation from ATL-146e, a highly selective adenosine A2A receptor agonist, in reperfused canine myocardi- um [ J]. Am J Physiol Heart Circ Physiol, 2005, 288 (4) : H1851 -H1858.
  • 10Jordan JE, Thourani VH, Auchampach JA, et al. A (3) adeno- sine receptor activation attenuates nentrophil funetion and neutro- phil-mediated reperfusion injury[ J]. Am J Physiol, 1999, 277 (5 Pt 2) : H1895-H1905.

引证文献1

二级引证文献3

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