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硫化氢对胃酸分泌的抗分泌作用及一氧化氮的参与

Antisecretory effect of hydrogen sulfide on gastric acid secretion and the involvement of nitric oxide.

作者信息

Mard Seyyed Ali, Askari Hasan, Neisi Niloofar, Veisi Ali

机构信息

Research Institute for Infectious Diseases of Digestive System, Physiology Research Center (PRC) and Department of Physiology, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.

Department of Physiology, The School of Medicine, Tehran University of Medical Sciences, Tehran, Iran ; Research Institute for Infectious Diseases of Digestive System, The School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357 15794, Iran.

出版信息

Biomed Res Int. 2014;2014:480921. doi: 10.1155/2014/480921. Epub 2014 Feb 24.

DOI:10.1155/2014/480921
PMID:24707486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3953662/
Abstract

The present study was designed to investigate the effect of H2S on distention-induced gastric acid secretion. Fifty-two rats were randomly assigned to seven experimental groups. The gastric acid secretion was stimulated by gastric distention. Two groups of rats received L-cysteine or saline for 5 days before stimulation of the gastric acid secretion. Two groups of animals also received NaHS or saline just prior to stimulation of the gastric acid secretion. The effect of L-NAME and propargylglycine was also investigated. The mucosal levels of the gene expression of cyclooxygenase-2 (COX-2), endothelial nitric oxide synthase (eNOS), and H(+)/K(+)-ATPase α-subunit were quantified by qPCR and luminal concentrations of NO were determined. NaHS and L-cysteine decreased the gastric acid output in response to distention. The mRNA expression of H(+)/K(+)-ATPase α-subunit decreased by NaHS and L-cysteine as compared with the control group while gene expression of eNOS and COX-2 was upregulated. The inhibitory effect of NaHS on distention-induced gastric acid secretion was mitigated by pretreatment of L-NAME. These findings suggest the involvement of NO in mediating the antisecretory effect of H2S.

摘要

本研究旨在探讨硫化氢（H2S）对扩张诱导的胃酸分泌的影响。52只大鼠被随机分为7个实验组。通过胃扩张刺激胃酸分泌。两组大鼠在胃酸分泌刺激前5天接受L-半胱氨酸或生理盐水。两组动物在胃酸分泌刺激前也接受硫氢化钠（NaHS）或生理盐水。还研究了L-硝基精氨酸甲酯（L-NAME）和炔丙基甘氨酸的作用。通过定量聚合酶链反应（qPCR）对环氧合酶-2（COX-2）、内皮型一氧化氮合酶（eNOS）和H(+)/K(+)-ATP酶α亚基的基因表达的黏膜水平进行定量，并测定一氧化氮（NO）的管腔浓度。NaHS和L-半胱氨酸可降低扩张引起的胃酸分泌量。与对照组相比，NaHS和L-半胱氨酸可使H(+)/K(+)-ATP酶α亚基的mRNA表达降低，而eNOS和COX-2的基因表达上调。L-NAME预处理可减轻NaHS对扩张诱导的胃酸分泌的抑制作用。这些发现表明NO参与介导H2S的抗分泌作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/acdc8ed81f45/BMRI2014-480921.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/21b382cf3752/BMRI2014-480921.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/638acbac9df4/BMRI2014-480921.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/ce6ae50d9e2d/BMRI2014-480921.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/790d39cfca25/BMRI2014-480921.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/94f32f466ca0/BMRI2014-480921.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/acdc8ed81f45/BMRI2014-480921.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/21b382cf3752/BMRI2014-480921.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/638acbac9df4/BMRI2014-480921.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/ce6ae50d9e2d/BMRI2014-480921.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/790d39cfca25/BMRI2014-480921.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/94f32f466ca0/BMRI2014-480921.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2593/3953662/acdc8ed81f45/BMRI2014-480921.006.jpg

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