期刊文献+

丙泊酚对大鼠脑缺血再灌注损伤的保护作用及其Caspase-3表达干预机制的研究 被引量:5

Protection of propofol on cerebral ischemia reperfusion injury in rats and its mechanism of intervention for Caspase-3
原文传递
导出
摘要 目的通过观察ip丙泊酚对脑缺血再灌注大鼠海马区神经细胞的影响,探讨丙泊酚对临床围手术期预防脑缺血再灌注损伤的作用。方法 SD大鼠60只随机分为丙泊酚组、假手术组和模型组。采用大脑中动脉线栓法制作左侧大脑动脉栓塞模型。在缺血再灌注前10 min时,丙泊酚组ip丙泊酚50 mg/kg,模型组ip给予等量生理盐水。假手术组只进行颈部切开、缝合操作而不进行缺血再灌注实验。缺血再灌注24 h采集脑组织。TTC染色法测定大鼠左侧脑组织梗死面积,免疫组化检测大鼠脑组织海马区Caspase-3的表达,原位杂交检测大鼠海马组织Caspase-3 m RNA的转录水平。结果与模型组比较,丙泊酚组脑组织灰白色区域明显缩小,改善了脑组织梗死面积,海马区Caspase-3的阳性表达和Caspase-3 m RNA的转录水平明显降低(P<0.01)。结论丙泊酚干预对大鼠脑缺血再灌注损伤有保护作用,其机制可能通过干预Caspase-3相关的细胞凋亡信号传导途径来完成。 Objective To observe the effects of propofol ip injection on hippocampus nervous after cerebral ischemia-reperfusion injury, to study the prevention of propofol to cerebral ischemia-reperfusion injury during clinical peroperative period.Methods Sixty SD rats were randomly divided into propofol group, Sham group, and model group. Left cerebral arterial embolism models were made. At 10 min before cerebral ischemia-reperfusion, rats in propofol group were ip administered propofol (50 mg/kg), and physiological saline was given to Sham group. Rats in model group were done the same operation except cerebral ischemia-reperfusion and propofol. At 24 h after ischemia reperfusion, the tissues were collected. The areas of left cerebral infarct of rats were measured by TTC staining method, Caspase-3 express in hippocampus was measured by immunohistochemical methods, and transcriptional levels of Caspase-3 mRNA were detected by in situ hybridization test.Results Compared with model group, gray area obviously shrank and incanus areas were improved in propofol group. The expression of Caspase-3 and transcriptional levels of Caspase-3 mRNA in hippocampus of rats in propofol group were lower than those in model group, with significant differences between two groups (P〈0.01). Conclusion Propofol intervention before ischemia-reperfusion maybe prevent ischemia reperfusion injury, and the mechanism is related to the apoptosis signal transduction pathway through Caspase-3 mediation.
出处 《现代药物与临床》 CAS 2015年第6期629-632,共4页 Drugs & Clinic
基金 河北省自然科学基金资助项目(H2012405016) 河北北方学院自然科学研究计划项目(120176)
关键词 丙泊酚 脑缺血再灌注 CASPASE-3 凋亡 propofol cerebral ischemia-reperfusion Caspase-3 apoptisis
  • 相关文献

参考文献12

  • 1Nakajima A, Tsuji M, Inagaki M, et al. Neuroprotective effects of propofol on ER stress-mediated apoptosis in neuroblastoma SH-SY5Y cells [J]. Eur J Pharmacol, 2014, 725: 47-54.
  • 2Longa E Z, Weinstein P R, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats [J]. Stroke, 1989, 20(1): 84-91.
  • 3Love S. Apoptosis and brain ischaemia [J]. Prog Neuropsychopharmacol Biol Psychiatry, 2003, 27(2): 267-282.
  • 4崔芳芹,杨卫东,陈前芬,赵云霞.不同时间脑缺血/再灌注损伤小鼠大脑Bcl-2和Caspase-3表达的变化[J].中国老年学杂志,2014,34(10):2765-2767. 被引量:7
  • 5Zhang X, Ha T, Lu C, et al. Poly (I:C) therapy decreases cerebral ischaemia/reperfusion injury via TLR3-mediated prevention of Fas/FADD interaction [J]. J Cell Mol Med, 2015, 19(3): 555-565.
  • 6Burguillos M A, Dejerborg T, Kavanagh E, et al. Caspase signalling controls microglia activation and neurotoxicity [J]. Nature, 2011, 472(7343): 319-324.
  • 7Zhou R, Yang Z, Tang X, et al. Propofol protects against focal cerebral ischemia via inhibition of microglia-mediated proinflammatory cytokines in a rat model of experimental stroke [J]. PLoS One, 2013, 8(12): e82729.
  • 8Basu S, Miclescu A, Sharma H, et al. Propofol mitigates systemic oxidative injury during experimental cardiopulmonary cerebral resuscitation [J]. Prostaglandins Leukot Essent Fatty Acids, 2011, 84(5/6): 123-130.
  • 9潘炳德,宋彩霞,杨堂斗,陈彦福,冯春声,刘波平,杨春燕.丙泊酚对大鼠局灶性脑缺血-再灌注时NF-κB活化和PUMA表达的影响[J].临床麻醉学杂志,2011,27(2):185-188. 被引量:2
  • 10Zhao X C, Zhang L M, Tong D Y, et al. Propofol increases expression of basic fibroblast growth factor after transient cerebral ischemia in rats [J]. Neurochem Res, 2013, 38(3): 530-537.

二级参考文献16

  • 1冯春生,麻海春,岳云,于洋,王云.异丙酚对大鼠局灶性脑缺血再灌注时NF-κB活化和Bcl-2、Caspase-3基因表达的影响[J].中华麻醉学杂志,2006,26(5):456-459. 被引量:16
  • 2赵玉鑫,王洪,杨述华,袁文旗.川芎嗪对大鼠脊髓损伤后caspase-3表达及细胞凋亡的影响[J].中国中医骨伤科杂志,2006,14(6):54-57. 被引量:15
  • 3Pulsinelli WA,JamesBA.New model of bilateral hemispheric ischemia in the unanesthetized rat[J].Stroke,1979,10:267.
  • 4Snyder GL,Galdi S,Hendrick J P,et al.general anaesthetics selectively modulate glutamatergic and dopaminergic signaling via site-specific phosphorylation in vivo[J].Neuropharmacology,2007,53(5):619-630.
  • 5Chen J,Graham SH,Chen PH,et al.Bcl-2 is expression in neurons that survive focal cerebral ischemia the rat[J].Neuroreport,1995,26(2):394-396.
  • 6Jeffers JR, Parganas E, Lee Y,et al. Puma is an essendal mediator of p53 dependent and independent apoptotic pathways. Cancer Gell, 2003,4 : 321-328.
  • 7Yu J, Wang Z, Kinzler KW, et al. PUMA mediales the apop totic response to p53 in colorectal cancer cells. Proc Natl Acad Sci USA,2003,100:1931-1936.
  • 8Bauer A, Villunger A, Labi V,et al. The NF kappaB regula tor Bcl 3 and the BH3only proteins Bim and Puma control the death of activated T cells. Proc Nail Acad Sci USA, 2006,103:10979-10984.
  • 9Wang P, Qiu W, Dudgeon C, et al. PUMA is directly activated by NFkappaB and contributes to TNF alphainduced apoptosis. Cell Death Differ,2009,16: 1192-1202.
  • 10Hunter AM, LaCasse EC, Korneluk RG. The inhibitors of apoplosis(IAPs) as cancer targets. Apoptos s,2007,12:1543-1568.

共引文献9

同被引文献43

引证文献5

二级引证文献35

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