期刊文献+

新生鼠缺氧缺血性脑损伤后水通道蛋白4表达与bFGF治疗效果的研究 被引量:1

Analysis of expression of AQP4 and treatment effects with bFGF on rats with hypoxia-ischemic brain damage
原文传递
导出
摘要 目的探讨新生大鼠缺氧缺血性脑损伤(hypoxic—ischemic brain damage,HIBD)后脑组织水通道蛋白(AQP4)基因与蛋白表达及碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)对HIBD治疗效果的影响。方法生后7d新生大鼠80只,随机分为正常对照组10只,HIBD组30只,bFGF治疗组(4μ/kg,腹腔注射,连续15d)30只,生理盐水治疗组10只。采用RT—PCR和蛋白印迹技术检测脑缺氧缺血后及经bFGF治疗不同时间段AQP4mRNA基因与蛋白的表达。结果HIBD后5h,脑组织AQP4mRNA表达增加;HIBD后7d达到高峰(1.93±0.11),15d后仍高于正常组织;HIBD后5h、3d.7d、15d、17d有不同程度的AQP4蛋白表达,3d、7d最为明显,而正常对照组未见蛋白表达。HIBE)后腹腔注射bFGF,3d后脑组织AQP4mRNA有明显变化(0.79±0.15),15d明显降低到(0.47±0.06);第7d蛋白表达逐渐减弱,15d、17d蛋白不表达。结论AQP4与HIBD的形成密切相关;bFGF对HIBD有明显的改善作用,可能与其保护作用有关。 Objective To study the expression of AQP4 in the hindbrain of neonatal rats with hypoxic-ischemic brain damage (HIBD) and to explore the effect of basic fibroblast growth factor (bFGF) on the treatment of HIBD. Methods Eighty neonatal rats aged 7-day were divided into randomly-control group ( 10 rats), HIBD group (30 rats), bFGF treated group (30 rats), and NS treated group (10 rats). HIBD were established by exposing rats to 92% N2 mixed with (8 ± 1) % O2 for 20 minutes after ligating the left carotis d the rats. bFGF treatel group were given bFGF 4u/kg for 15 days via intraperitoneal injection. The expression of AQP4 mRNA and AQP4 protein of neonatal rats with HIBD were examined with RT-PCR and Western blotting at different stage after hypoxia. Results In HIBD group, the expression of AQP4 mRNA in hindbrain was higher than that in control group at 5 h after HIBD. reached peak at 7 d ( 1.93 ± 0.11 ) after hypoxia, and remained at a high level until 15 d ( 1.41 ± 0.23) after hypoxia. In bFGF group, the expression of AQP4 mRNA in hindbrain was obviously changed at 3 d (0.79 ± 0.15) after hypoxia, decreased evidently at 15 d (0.47 ±0.06). In bFGF group, the expressions of AQP4 protein at 5 h, 3 d. 7 d after HIBD were positive at different degree, with the decreasing level at 7 d and no protein at 15 d and 17 d. Meanwhile, the expressions in normal control group were negative. Conclusion AQP4 was closely related with the formation of HIBD. After treating with bFGF HIBD can improved significantly, which may be due to the protection role of bFGF.
出处 《中国小儿急救医学》 CAS 2008年第1期58-60,共3页 Chinese Pediatric Emergency Medicine
关键词 缺氧缺血性脑损伤 水通道蛋白 碱性成纤维细胞生长因子 蛋白印迹技术 Hypoxia-ischemic brain damage Aquaporin:Basic fibroblast growth factor Western blotting
  • 相关文献

参考文献2

二级参考文献12

  • 1Wagner KR,Xi G,Hua Y,et a.Ultra-early clot aspiration after lysis with tissue plasminogen activator in a pig intracerebral model.Edema re duction and blood barrier protection.J Neurosurg,1999,90:491
  • 2Cherubini A,Polidori MC,Brebnocchi M,et al.Antioxidant profile and early outcome in stroke patients.Stroke,2000,31:2295
  • 3Wagner KR,Xi G,Hua Y,et al.Early metabolic alteratrions in edematous perihematomal brain regions following experimental intracerebral hemorrhage.J Neurosurg,1998,88:1058
  • 4Lee KR,Kawai N,Kim S,et a.Mechanisms of edema formation after intracerebral hemorrhage:Effects of thrombin on cerebral blood flow,blood-brain barrier permeability,and cell survival in a rat model.J Neurosurg,1997,86:272
  • 5Xue M,Del B.Acute tissue damage after injection of thrombin and plasmin into rat striatum.Stroke,2001,32:2164
  • 6Belayev L,Busto R,Zhao W,et al.Quantitative evaluation of blood-brain barrier permeability following middle cerebral artery occlusion in rats.Brain Research,1996,739:88
  • 7Kimelberg HK.Current concepts of brain edema.Review of laboratory investigations.J Neurosurg,1995,83:1051
  • 8Smith SL,Scherch HM,Hall ED.Protective effects of tirilazad me sylate and metabolite U-89678 agaist blood-brain barrier damage after suba-rachnoid hemorrhage and lipid peroxidative neuronal injury.J Neurosurg,1996,84:229
  • 9程保和.脑血管疾病的预防,见:韩仲岩主编.实用脑血管疾病学.上海:上海科学技术出版社,1996,424
  • 10宫晔,陈衔城,鲍伟民.脑出血后脑组织水、离子变化及水蛭素的作用[J].上海医科大学学报,2000,27(2):105-107. 被引量:19

共引文献42

同被引文献14

  • 1Tanaka M, Natori M, Ishimoto H, et al. Experimental growth re- tardation produced by transient period of uteroplacental ischemia in pregnant Sprague-Dawley rat. Am J Obstet Gynecol, 1994, 171 (5) : 1231-1234.
  • 2Leone TA, Finer NN. Shock: A common consequence of neo- natal asphyxia. J Pediatr,2011,158(2 suppl) :e9-12.
  • 3Sun HY, Wang NP, Kerendi F, et al. Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2 ~ overload. Am J Physiol Heart Circ Physiol, 2005,288 (4) : H1900-1908.
  • 4Gaze DC, Collinson PO. Multiple molecular forms of circulating cardiac troponin: analytical and clinical significance. Ann Clin Biochem,2008,45 ( Pt 4 ) : 349-355.
  • 5Lesnefsky E J, Moghaddas S, Tandler B, et al. Mitochondrial dysfunction in cardiac disease : ischemia--reperfusion, aging, and heart failure. J Mol Cell Cardiol,2001,33 (6) :1065-1089.
  • 6Di Lisa F, Bernardi P. Mitochondria and ischemia-reperfusion injury of the heart:Fixing a hole. Cardiovasc Res ,2006,70 (2) : 191-199.
  • 7Hunter DR, Haworth RA, Southard H. Relationship between configuration, function, and permeability in calcium-treated mi- tochondria. J Biol Chem, 1976,251 (16) :5069-5077.
  • 8Crompton M, Costi A, Hayat L. Evidence for the presence of a reversible Ca2 dependent pore activated by oxidative stress in heart mitochondria. Biochem J, 1987,245 ( 3 ) : 915-918.
  • 9Petronilli V, Penzo D, Scorrano L. The mitochondrial permea- bility transition, release of cytochrome c and cell death. J Biol Chem,2001,276( 15 ) : 12030-12034.
  • 10Otera H, Ohsakaya S ,Nagaura Z,et al. Export of mitochondrial AIF in response to proapoptotic stimuli depends on processing at the inter membrane space. EMBO J, 2005,24 ( 7 ) : 1375-1386.

引证文献1

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