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A Study on Mechanisms of Exacerbation of Indomethacin-lnduced Gastric Ulcer by GABA in Mice

Xu Xianggui ( Department of Biology )  
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 ( p0.01), 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(p0.05). 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.
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