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电压门控钠通道亚单位在大鼠肠易激综合征模型中变化的研究 被引量:7

Alteration of α-Subunit of Voltage-gated Sodium Channels in a Rat Model of Irritable Bowel Syndrome
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摘要 背景:电压门控钠通道(VGSC)在神经元动作电位的产生和传递中起着极为重要的作用。近年来它与内脏高敏感性的关系越来越受到重视。目的:探讨VGSC亚单位的变化与大鼠肠易激综合征(IBS)内脏高敏感性之间的关系。方法:以新生大鼠直肠内气囊扩张制作IBS的动物模型,在其成年后取L6-S2脊髓背根神经节,采用逆转录聚合酶链反应(RT-PCR)半定量法对背根神经节细胞表面VGSCNav1.1、Nav1.6、Nav1.7、Nav1.8和Nav1.9五种α亚单位mRNA的含量进行检测,并以原位杂交的方法对Nav1.8的表达进一步加以确认;采用酶联免疫吸附试验(ELISA)法对大鼠肠道组织神经生长因子(NGF)的含量进行检测。结果:背根神经节细胞表面α亚单位Nav1.8mRNA的表达增加,而Nav1.1、Nav1.6、Nav1.7和Nav1.9的表达没有改变,原位杂交定性分析也证实造模组Nav1.8含量增加;造模组肠道组织NGF的含量显著高于对照组。结论:新生大鼠直肠内气囊扩张使其脊髓背根神经节细胞Nav1.8mRNA的表达增加,而其他几种常见α亚单位的含量均未发生改变。这种变化可能与肠道组织NGF表达的增加有关。 Background: Voltage-gated sodium channels (VGSC) are crucial for the generation and propagation of action potentials. Some researchers suggested that voltage-gated sodium channels were altered in many gastrointestinal diseases. Aims: To determine which voltage-gated sodium channel is involved in visceral hypersensitivity of irritable bowel syndrome (IBS). Methods: An animal model of IBS was established by giving rectal balloon distension in the neonatal Sprague-Dawley rats on postnatal days 8, 10 and 12. The L6~S2 dorsal root ganglia were removed after entering adulthood. The expressions of five α-subunits of VGSC: Nav1.1, Nav1.6, Nav1.7, Nav1.8 and Nav1.9 mRNAs in the dorsal root ganglion neurons were detected by reverse transcription polymerase chain reaction (RT-PCR), and the increased expression of Nav1.8 was confirmed by in situ hybridization (ISH). Nerve growth factor (NGF) expression in colon tissue was measured by enzyme linked immunosorbent assay (ELISA). Results: Among the five α-subunits of VGSC examined, only expression of Nav1.8 mRNA was higher in neonatal rectal distension group than that in the control group. The model rats bad more NGF in colon tissue than in the controls. Conclusions: Neonatal rectal balloon distension treatment in mice may alter the expression of α-subunit Nav1.8, which may be associated with increase of NGF in the colon tissue.
出处 《胃肠病学》 2006年第3期143-147,共5页 Chinese Journal of Gastroenterology
基金 国家自然科学基金项目(No.30570830)资助
关键词 大鼠 肠易激综合征 内脏高敏感性 电压门控钠通道 神经生长因子 Rats Irritable Bowel Syndrome Visceral Hypersensitivity Voltage-Gated Sodium Channel Nerve Growth Factor
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参考文献19

  • 1Bielefeldt K,Ozaki N,Gebhart GF.Experimental ulcers alter voltage-sensitive sodium currents in rat gastric sensory neurons.Gastroenterology,2002,122:394~405.
  • 2Bielefeldt K,Ozaki N,Gebhart GF.Mild gastritis alters voltage-sensitive sodium currents in gastric sensory neurons in rats.Gastroenterology,2002,122:752~761.
  • 3Moore BA,Stewart TM,Hill C,Vanner SJ.TNBS ileitis evokes hyperexcitability and changes in ionic membrane properties of nociceptive DRG neurons.Am J Physiol Gastrointest Liver Physiol,2002,282:G1045~G1051.
  • 4王亚雷,袁耀宗,徐天乐.电压门控钠离子通道在大鼠肠易激综合征模型中的变化[J].诊断学理论与实践,2005,4(2):140-144. 被引量:7
  • 5Lin C,Al-Chaer ED.Long-term sensitization of primary afferents in adult rats exposed to neonatal colon pain.Brain Res,2003,971:73~82.
  • 6Goldin AL.Resurgence of sodium channel research..Annu Rev Physiol,2001,63:871~894.
  • 7Black JA,Dib-Hajj S,McNabola K,Jeste S,Rizzo MA,Kocsis JD,Waxman SG.Spinal sensory neurons express multiple sodium channel alpha-subunit mRNAs.Brain Res Mol Brain Res,1996,43:117~131.
  • 8Gold MS.Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia.Proc Natl Acad Sci U S A,1999,96:7645~7649.
  • 9Lai J,Gold MS,Kim CS,Bian D,Ossipov MH,Hunter JC,Porreca F.Inhibition of neuropathic pain by decreased expression of the tetrodotoxin-resistant sodium channel,NaV1.8.Pain,2002,95:143~152.
  • 10Gold MS,Zhang L,Wrigley DL,Traub RJ.Prostaglandin E (2) modulates TTX-R I (Na) in rat colonic sensory neurons.J Neurophysiol,2002,88:1512~1522.

二级参考文献17

  • 1[1]Bielefeldt K, Ozaki N, Gebhart GF. Experimental ulcers alter voltage-sensitive sodium currents in rat gastric sensory neurons[J]. Gastroenterology, 2002,122(2):394-405.
  • 2[2]Bielefeldt K, Ozaki N, Gebhart GF. Mild gastritis alters voltage-sensitive sodium currents in gastric sensory neurons in rats[J]. Gastroenterology, 2002,122(3):752-761.
  • 3[3]Moore BA, Stewart TM, Hill C, et al. TNBS ileitis evokes hyperexcitability and changes in ionic membrane properties of nociceptive DRG neurons [J]. Am J Physiol Gastrointest Liver Physiol, 2002,282(6):G1045-G1051.
  • 4[4]Lin C, Al-Chaer ED. Long-term sensitization of primary afferents in adult rats exposed to neonatal colon pain [J].Brain Res, 2003,971(1):73-82.
  • 5[5]Dong XP, Xu TL. Radix paeoniae rubra suppression of sodium current in acutely dissociated rat hippocampal CA1 neurons[J]. Brain Res,2002,940(1-2):1-9.
  • 6[6]Mayer EA, Collins SM. Evolving pathophysiologic models of functional gastrointestinal disorders[J]. Gastroenterology, 2002,122(7):2032-2048.
  • 7[7]Al-Chaer ED, Kawasaki M, Pasricha PJ. A new model of chronic visceral hypersensitivity in adult rats induced by colon irritation during postnatal development [J]. Gastroenterology, 2000,119(5):1276-1285.
  • 8[8]Al-Chaer ED,Traub RJ. Biological basis of visceral pain:recent developments[J]. Pain, 2002,96(3):221-225.
  • 9[10]McCleskey EW,Gold MS. Ion channels of nociception[J].Annu Rev Physiol, 1999,61:835-856.
  • 10[11]Yoshimura N,Seki S, Novakovic SD, et al .The Involvement of the tetrodotoxin-resistant sodium channel Nav1.8(PN3/SNS) in a rat model of visceral pain[J]. J Neurosci,2001,21 (21 ):8690-8696.

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