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兴奋性氨基酸对小鼠冷束缚应激诱导胃溃疡的保护作用:环核苷酸的作用

Protective effect of excitatory amino acids on cold-restraint stress-induced gastric ulcers in mice: role of cyclic nucleotides.

作者信息

Chen S H, Lei H L, Huang L R, Tsai L H

机构信息

Department of Internal Medicine College of Medicine, Taipei Medical University, Taiwan.

出版信息

Dig Dis Sci. 2001 Oct;46(10):2285-91. doi: 10.1023/a:1011991721640.

Abstract

Previous studies have shown that excitatory amino acids (EAAs) and their receptors may play important roles in the mammalian enteric system. In this study, we investigated whether EEAs, including L-glutamate (L-Glu) and subtypes N-methyl-D-aspartate (NMDA), kainic acid (KA), and quisqualic acid (QA), reduce cyclic AMP (cAMP) levels and play a role in protecting gastric lesions in cold-restraint stress (CRS) mice. First, we found that dose-dependent administration of four selected EAAs significantly attenuated the increase of cAMP content and exhibited a protective effect on the development of gastric lesions induced by CRS. Second, CRS treatment exhibited a decrease of cGMP content and an increase of cAMP content with marked time-dependent changes, and a high cAMP/cGMP ratio in mice gastric mucosa. Third, pretreatment with 0.25 microg/kg or 0.5 microg/kg dibutyryl cGMP (db-cGMP) exhibited protective effects on CRS-induced gastric lesions, with preventive ratios of 24.61% and 35.32%, respectively. Moreover, db-cGMP at 0.5 microgg/kg significantly attenuated the increase in both cAMP content and the cAMP/cGMP ratio in CRS-treated gastric mucosa. In contrast, db-cAMP exhibited no protective effect, and significantly decreased cGMP content and increased the cAMP/cGMP ratio. These results suggest that EAAs significantly reduce CRS-induced gastric ulcers in mice. The possible mechanism of the antiulcer activity of EAAs may be related to a decrease in the cAMP content in the gastric mucosa of mice. In addition, an increase of the cAMP/cGMP ratio significantly involved in CRS-induced gastric ulcer formation in mice.

摘要

先前的研究表明,兴奋性氨基酸(EAAs)及其受体可能在哺乳动物肠道系统中发挥重要作用。在本研究中,我们调查了包括L-谷氨酸(L-Glu)以及N-甲基-D-天冬氨酸(NMDA)、 kainic酸(KA)和quisqualic酸(QA)亚型在内的兴奋性氨基酸是否会降低环磷酸腺苷(cAMP)水平,并在冷束缚应激(CRS)小鼠的胃损伤保护中发挥作用。首先,我们发现对四种选定的兴奋性氨基酸进行剂量依赖性给药可显著减弱cAMP含量的增加,并对CRS诱导的胃损伤发展具有保护作用。其次,CRS处理导致小鼠胃黏膜中cGMP含量降低、cAMP含量增加,并呈现出明显的时间依赖性变化,以及较高的cAMP/cGMP比值。第三,用0.25μg/kg或0.5μg/kg二丁酰环磷鸟苷(db-cGMP)进行预处理对CRS诱导的胃损伤具有保护作用,预防率分别为24.61%和35.32%。此外,0.5μg/kg的db-cGMP显著减弱了CRS处理的胃黏膜中cAMP含量和cAMP/cGMP比值的增加。相比之下,db-cAMP没有保护作用,且显著降低了cGMP含量并增加了cAMP/cGMP比值。这些结果表明,兴奋性氨基酸可显著减轻CRS诱导的小鼠胃溃疡。兴奋性氨基酸抗溃疡活性的可能机制可能与小鼠胃黏膜中cAMP含量的降低有关。此外,cAMP/cGMP比值的增加在CRS诱导的小鼠胃溃疡形成中起重要作用。

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