摘要
本工作初步分析脑室注射GABA加剧小鼠消炎痛-胃溃疡的机制,结果如下:(1)脑室注射GABA可显著加剧小鼠消炎痛-胃溃疡的发生(p<0.01),而腹腔注射GABA(100μmol)对消炎痛-胃溃疡则无影响。 (2)脑室注射GABA_A受体阻断剂荷包牡丹碱能显著抑制消炎痛-胃溃疡(p<0.01)。脑室注射GABA_B受体激动剂β-氯苯基-γ-氨基丁酸则显著加剧消炎痛-胃溃疡(p<0.05)。荷包牧丹碱不能改变脑室注射GABA和β-氟苯基-γ-氖基丁酸加剧消炎痛-胃溃疡的效应。 (3)皮下注射胆碱能神经M受体阻断剂阿托品使消炎痛-胃溃疡明显加重(p<0.01),阿托品可部分阻断GABA对消炎痛-胃溃疡的加剧效应。 (4)肌肉注射肾上腺素能神经α受体阻断剂酚妥拉明不影响消炎痛-胃溃疡的发生,也不改变GABA对消炎痛-胃溃疡的加剧效应。 以上这些结果表明:外源性GABA可能通过中枢的特异性机制加剧消炎痛-胃溃疡。脑中GABA_A和GABA_B受体与消炎痛-胃溃疡的发生都有关,激活GABA_B受体可能是GABA加剧消炎痛-胃溃疡的重要机制。迷走神经在胃粘膜的保护机制中可能起一定的作用,它可能是GABA通过中枢加剧消炎痛-胃溃疡发生的途径之一。
The paper studied the mechanisms that administering GABA to intracerebroventricular exacerbated gastric ulcer induced by indomethacin in mice. The results were as follows:
( 1 )GABA( i. c. v. ) significantly exacerbated the development of gastric ulcer induced by indomethacin ( p<0.01), while intraperitoneal injection ( i. p. ) of GABA( 1200μmol ) did not alter indomethacin-induced gastric ulcer ( IGU).
( 2 ) Bicuculline ( i.c.v. 0.2μmol ) , a blocker of GABAAreCeptor, inhlbited I G U significantly ( p <0.01 ). Whereas baclofen ( i.c.v. 4μmol), a GABAB agonist, significantly exacerbated IGU(p<0.05). Bicuculline did not modify the exacerbation of I G U by GABA and baclofen.
( 3) Atropine(S.C. 0.2mg/kg ) markedly promoted I G U ( p <0.01 ), and partially blocked the exacerbation of I G U by GABA.
( 1 ) Regetine ( i.m. 2.5mg/kg ) did not effect the development of IG U, and did not modify the above ulcerogenic effect of GABA.
Above those results showed that extragenetic GABA exacerbated I G U through special central GABAergic mechanisms, but no peripherally. The activities of both GABAA and GABAB receptors related to the development of IGU, possibly it was the important mechanism through which GABA exacerbated IGU that activiting GABAB recepter.Possibly vagus contributed to gastric protective effect against IGU and was a pathway through which GABA exacerbated IGU after effecting CNS.
出处
《苏州科技学院学报（社会科学版）》
1992年第S1期42-49,共8页
Journal of University of Science and Technology of Suzhou:Social Science
