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反复热性惊厥过程中γ-氨基丁酸B受体对气体信号分子一氧化碳的影响 被引量:5

Influence of Gamma-Aminobutyric Acid B Receptor on Expression of Carbon Monoxide/ Heme Oxygenase System during Recurrent Febrile Seizures
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摘要 目的探讨γ氨基丁酸B受体(GABABR)对热性惊厥(FS)大鼠一氧化碳(CO)/血红素氧合酶(HO)系统表达的影响。方法SD大鼠32只随机分为对照组、FS组、FS+baclofen组、FS+phaclofen组,每组各8只。采用热水浴诱导大鼠FS,隔日诱导1次,共10次。采用双波长分光光度计法测定大鼠血浆CO含量;用原位杂交观察GABABR和HO1mRNA表达情况;用免疫组织化学方法观察GABABR和HO1蛋白表达情况。结果FS+baclofen组CO含量高于FS组,同时HO1表达也较FS组增强;而FS+phaclofen组CO含量低于FS组,同时HO1表达也较FS组减弱。FS+baclofen组和FS+phaclofen组与FS组相比,差异均有显著意义(P均<0.05)。结论反复FS过程中,GABABR的改变可影响CO/HO1系统的表达。 Abstract: Objective To explore the influence of γ-aminobutyric acid B receptor(GABABR)on carbon monoxide (CO)/heme oxygenase(HO - 1 )system during recurrent febrile seizures (FS). Methods Sprague Dawley rats aged 21 days were randomly divided into 4 groups: control group and FS group, FS + baclofen group, FS + phaclofen group. FS in rats were induced 10 times in a bath of wama water, once every 2 days. The plasma level of CO was detected by the dual wave lengh spectrophotometer; the expressions of GABABR and HO 1 mRNA were examined by insitu hybridization; the expressions of GABABR and HO- 1 protein were observed by immunohistochernistry. Results The plasma level of CO increased in FS + baclofen group, while decreased in FS + phaclofen group compared with FS group, The expressions of GABABR and HO 1 upregulated in FS+ baclofen group, while decreased in FS + pha- clofen group compared with FS group. There were significant difference (All P〈 0.05). Conclusion GABABR can modulate the expression of CO/HO- 1 system during recurrent FS.
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2005年第12期1229-1231,I0058,共4页 Journal of Applied Clinical Pediatrics
基金 卫生部临床学科重点基金项目资助(20010912)
关键词 惊厥 发热性 γ-氨基丁酸 受体 一氧化碳 血红素氧合酶 scizure, febrile gamma - aminobutyric acid receptor carbon monoxide heine oxygenase
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  • 1乐宏元,宋小兴,刘和平.一氧化碳血红蛋白双波长定量测量[J].临床检验杂志,1996,14(2):87-88. 被引量:92
  • 2[1]Cutaia M, Rounds S. Hypoxic pulmonary vasoconstriction. Physiologic significance, mechanism, and clinical relevance[J]. Chest, 1990;97(3) :706~718
  • 3[2]Dzau VJ,Gibbons GH. Vascular remodeling: mechanisms and implications[ J ]. J Cardiovascular Pharmacol, 1993; 21 (Suppl. 1 ): S1~S5
  • 4[3]Fujio Y, Yamada F, Takahushi k, et al. Altered fibronectin-dependent cell adhesion by PDGF accompanies phenotypic modulation of vascular smooth muscle cells [ J ]. Biochem Biophys Res Commun,1993; 196(2): 997~1002
  • 5[4]Kourembanas S,Bemfield M. Hypoxia and endothelial-smooth muscle cell interactions in the lung[J]. Am J Respir Cell Mol Biol, 1994; 11:373 ~374
  • 6[5]Marines MD. The heme oxygenase system: a regulator of second messenger gases[J]. Annu Rev Pharmacol Toxicol, 1997;37:517~554
  • 7[6]Yu AY, Frid MG,Shirmoda LA, et al. Temporal spatial and oxygenregulated expression of hypoxia-inducible factor-1 in the lung[J]. Am J Physiol, 1998; 275: L818
  • 8[7]Morita T, Kourembanas S. Endothelial cell expression of vasoconstrictors and growth factors is regulated by smooth muscle cell-derived carbon rmonoxide[J ]. J Clin Invest, 1995 ;96(6) :2676~2682
  • 9[8]Morita T, Mitsialis SA, Koike H, et al. Carbon monoxide controls the proliferation of hypoxic vascular smooth muscle cells [ J ]. J Biol Chem, 1997;272 (52) :32804~32809
  • 10[9]Christ6u H, Morita T, Hsieh CM, et al. Prevention of hypoxia-induced pulmonary hypertension by enhancement of endogenous heme oxygenase-1 in the rat[J]. Circ Res,2000;86:1224~ 1229

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