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徐项桂, 朱剑琴, 王学庆. 1992: GABA对乙醇诱导型胃溃疡的影响及其机制分析. 动物学研究, 13(2): 139-144.
引用本文: 徐项桂, 朱剑琴, 王学庆. 1992: GABA对乙醇诱导型胃溃疡的影响及其机制分析. 动物学研究, 13(2): 139-144.
XU Xiang-gui, ZHU Jian-qin, WANG Xue-qin. 1992. Effect of Intracerebroventricular Injection of GABA on Ethanol-Induced Gastric Ulcer in Mice. Zoological Research, 13(2): 139-144.
Citation: XU Xiang-gui, ZHU Jian-qin, WANG Xue-qin. 1992. Effect of Intracerebroventricular Injection of GABA on Ethanol-Induced Gastric Ulcer in Mice. Zoological Research, 13(2): 139-144.

GABA对乙醇诱导型胃溃疡的影响及其机制分析

Effect of Intracerebroventricular Injection of GABA on Ethanol-Induced Gastric Ulcer in Mice

  • 摘要: 小白鼠脑室注射不同浓度GABA(2、4、6 umol)对乙醇诱导型溃疡有显著的促进作用,且有明显的剂量-效应关系。腹腔注射GABA(100 umol)则对乙醇诱导型胃溃疡没有影响;阿托品(s.c.0.2 mg/kg)使溃疡明显加重,阿托品(s.c.0.2 mg/kg)加GABA(I.c.v.4 umol)使溃疡比单独注射GABA时减轻41%;酚妥拉明(I.m.2.5 mg/kg)对溃疡发生没有影响,酚妥拉明(I.m.2.5 mg/kg)加GABA(I.c.v.4 umol)不改变单独注射GABA时的促溃疡效应。以上结果提示,外源性GABA通过中枢机制可加剧乙醇诱导型胃溃疡的发生;迷走神经可能在胃的自身保护机制中起重要调节作用,而交感神经可能无作用;中枢GABA并不通过交感神经,而可能通过迷走神经及其他途径加剧了乙醇诱导型胃溃疡的发生。

     

    Abstract: Intracerebroventricularly (I.c.v.) administered GABA (2.4.6 umol) significantly accelerated the development of gastric ulcer induced by ethanol (o.p.) in mice in a dose dependent manner,whereas GABA (I.p.100 umol) could not modify the ethanol-induced ulcer in mice.Atropine (s.e.0.2 mg/kg) exacerbated the ethanol-induced ulcer significantly,while blocking the exacerbation of ulcer induced by GABA partly.Regetine (I.m.2.5 mg/kg) potentiated the ethanol-induced ulcer weakly,and had no effect on the exacerbation of ulcer induced by GABA.These results suggested that exsragenetic GABA exacerbates the ethanolinduced gastric ulcer through central GABA-ergic mechanisms,but not peripherally.Vagus may contribute to gastric protective effect against ulceration.It may be one of main pathway in GABA s action.Sympathetic nerve maybe have relationship with the GABA-ergic mechanisms.

     

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