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尼莫地平对过氧化氢诱导猪脑基底动脉氧化应激损伤的保护作用 被引量:9

Protective effect of Nimodipine on porcine basilar artery oxidative stress injury induced by hydrogen peroxide
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摘要 目的:探讨尼莫地平对过氧化氢(H2O2)诱导猪脑基底动脉损伤的保护作用。方法:采用去内皮离体血管环灌流的方法,建立H2O2损伤模型。比较正常对照组,H2O2(2×10-4mol/L)损伤组,维生素C(10-4mol/L)组,尼莫地平高、中、低剂量(5×10-6、5×10-7、5×10-8mol/L)组血管环对KCl、苯肾上腺素的张力;检测各组血管组织匀浆中的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)活性及丙二醛(MDA)含量。结果:(1)H2O2损伤组与正常对照组比较,血管环对KCl、苯肾上腺素的收缩反应明显增加;尼莫地平高、中、低剂量组呈剂量依赖性抑制KCl、苯肾上腺素对血管环的收缩反应。(2)H2O2损伤组MDA含量升高,SOD、CAT、GSH-PX活性降低,与正常对照组比较,差异有统计学意义(P<0.05)。尼莫地平高、中、低剂量均能降低组织中MDA含量,增强SOD、CAT、GSH-PX的活性,与H2O2损伤组比较,差异有统计学意义(P<0.05)。结论:钙通道阻断剂尼莫地平具有抗氧化应激作用,能预防H2O2对脑基底动脉血管的氧化损伤。 AIM: To study the protective effect of Nimodipine on porcine basilar artery oxidative stress injury induced by hydrogen peroxide ( H2O2 ). METHODS: Porcine basilar artery rings without endothelium were isolated and allocated in 6 groups: control, H2O2(2 ×10^-4 mol/L) injury, Vitamin C(10^-4 mol/L) pretreatment, Nimodipine with high , moderate and low dose pretreatment (5 ×10^-6, 5×10^-7, 5×10^-8 mol/L),which were handled with organ chamber technique. The tensive changes after they were treated by vaso-excitor material KCl, phenylephrine and H2O2 were compared and the activity changes of superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT) and glutathione peroxidase (GSH-PX) were detected. RESULTS: (1) Compared with those in the control group, the vascular ring of the H2O2 injury group showed more significant contractile response to KCl and phenylephrine. Nimodipine with high, moderate and low doses pretreatment inhibitted the contractile response of the vascular ring to KCl and phenylephrine in dose dependent. (2)Compared with those in the control group, the content of MDA in H2O2 injury group was increased, and the activities of SOD, CAT, GSH-PX were degraded. They all have significant difference ( P 〈 0.05). Compared with the control group, Nimodipine with high, moderate and low doses pretreatment all degraded the content of MDA, and increased the activity of SOD, CAT, GSH-PX. They all had significant difference ( P 〈 0.05). CONCLUSION: Nimodipine can inhibit the contraction of vascular and prevent brain arteria basilaris from injuring.
出处 《中国临床药理学与治疗学》 CAS CSCD 2007年第8期906-910,共5页 Chinese Journal of Clinical Pharmacology and Therapeutics
关键词 尼莫地平 过氧化氢 基底动脉 氧自由基 血管平滑肌细胞 Nimodipine hydrogen peroxide basilar artery oxygen free radical vascular smooth muscle cell
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参考文献12

  • 1Touyz RM,Schiffrin EL.Reactive oxygen species in vascular biology:implications in hypertension[J].Histochem Cell Biol,2004;122:339-352.
  • 2Ardanaz N,Pagano PJ.Hydrogen peroxide as a paracrine vascular mediator:regulation and signaling leading to dysfunction[J].Exp Biol Med (Maywood),2006;231:237-251.
  • 3Li J,Li W,Su J,et al.Hydrogen peroxide induces apoptosis in cerebral vascular smooth muscle cells:possible relation to neurodegenerative diseases and strokes[J].Brain Res Bull,2003;15,62:101-106.
  • 4Yang ZW,Zheng T,Wang J,et al.Hydrogen peroxide induces contraction and raises[Ca2+] in canine cerebral arterial smooth muscle:participation of cellular signaling pathways[J].Naunyn Schmiedebergs Arch Pharmacol,1999;360:646-653.
  • 5Iida Y,Katusic ZS.Mechanisms of cerebral arterial relaxations to hydrogen peroxide[J].Stroke,2000;31:2224-2230.
  • 6Kim CJ,Kim kw,Park JW,et al.Role of Ca(2+)-dependent K+ channels in erythrocyte lysate-induced contraction of rabbit cerebral artery[J].Neurol Res,1999;21:705-711.
  • 7Brian JE Jr,Heistad DD,Faraci FM.Effect of carbon monoxide on rabbit cerebral arteries[J].Stroke,1994;25:639-643.
  • 8刘欣,刘先义.细胞凋亡与氧自由基[J].湖北民族学院学报(医学版),2002,19(4):31-33. 被引量:16
  • 9Tabet F,Savoia C,Schiffrin EL,et al.Differential calcium regulation by hydrogen peroxide and superoxide in vascular smooth muscle cells from spontaneously hypertensive rats[J].J Cardiovasc Pharmacol,2004;44:200-208.
  • 10Touyz RM.Reactive oxygen species and angiotensin II signaling in vascular cells-implications in cardiovascular disease[J].Braz J Med Biol Res,2004;37:1263-1273.

二级参考文献22

  • 1Henschke PN, Flliott S. Oxidized glutathione decrease luminal Ca2+ content of the endothelial cell ins(1,4,5)p3- sensitive Ca2+ store[J].Biochem J.1995,312:485~ 489
  • 2Gopalakrishna R, Anderson WB.Reversible oxidative activation and inactivation of protein kinase c by the mitogen /tumor promoter periodate[J].Arch Biochem Biophys.1991,285:382~ 387.
  • 3Chen Y, Yang DC, Brown AB .Activation of a membrane- associated phosphatidylinositol kinase through tyrosine- protein phosphorylation by Naphthoquinones and Orthovanadate[J]. Arch Biochem Biophys.1990,283:184~ 188
  • 4Sreedha AS, Pardhasaradhi BV, Khar A, et al. Heat- induced expression of CD95 and its correlation with the activation of apoptosis upon heat shock in rat histiocytic tumor cells[J]. FEBS Lett.2000,472:271~ 275
  • 5Munisch D, Watanabe- Fukunaga R, Bourdon J, et al.Human and Mouse Fas(Apo- 1/CD95) death receptor genes each contain a p53- responsive element that is activated by p53 mutants unable to induce apoptosis[J]. J.Biol.chem..2000,275 :3867~ 3872
  • 6Ashkenazi A. Dixit VM.Death receptors:signaling and modulation[J]. J.Science.1998,281(5381): 1305~ 1308
  • 7Sreedhar AS, Pardhasaradhi BV, Khar A, et al. A cross talk between cellular signaling and cellular redox state during heat- induced apoptosis in a rat histiocytoma[J]. Free Radical Biology and Medicine. 2002,32(3):221~ 227
  • 8Lemaster JJ, Nieminen AL, QianT, et al. The mitochondrial permeability transition in cell death:a common mechanism ,apoptosis and autophagy[J]. Biochem Biophysi Acta.1998,1366 (1- 2):177~ 196
  • 9Koremer G, Zamzami N, Susin SA. Mitochondrial control of nuclear apoptosis[J]. Immunology Today.1997,18(1):41~ 50
  • 10Cain K, Bratton SB, Langlais C, et al.Apaf- 1 oligomerizes into bioiogically active approximately700- Kda and inactive approximately 1.4- Mda apoptosome complexes[J]. J.Biolchem.2000,275(9):6067~ 6070

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