| 胃粘膜Na~+-K~+-Mg~(2+)-ATPase在适应性细胞保护机制中的作用 |
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| 引用本文： | 汪建英,王志均.胃粘膜Na~+-K~+-Mg~(2+)-ATPase在适应性细胞保护机制中的作用[J].生理学报,1988,40(3):215-222. |
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| 作者姓名： | 汪建英 王志均 |
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| 作者单位： | 北京医科大学基础医学研究所消化、生殖生理研究室，北京医科大学基础医学研究所消化、生殖生理研究室 日本京都药科大学应用药理教研室 |
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| 摘 要： | 本文观察了胃粘膜(Na~+-K~+-Mg~(2+))-ATPase在适应性细胞保护机制中的作用,并分析了其与内源性PG的关系。结果表明,哇巴因(一种(Na~+-K~+-Mg~(2+))-ATPase的抑制剂)可部分抑制胃蛋白酶150U(溶于0.1mol/L盐酸中)和20％乙醇的适应性细胞保护作用,并呈现明显的量效关系。用上述两种弱刺激灌胃后15min,胃粘膜(Na~+-K~+-Mg~(2+))-ATPase活力明显升高,也呈现明显的量效关系。预先给予消炎痛以抑制内源性PG的合成,则可阻断弱刺激所诱发的胃粘膜(Na~+-K~+-Mg~(2+))-ATPase活力的升高;若在此基础上再给予外源性PGE_2,又可解除消炎痛的阻断作用。这些结果说明,弱刺激通过内源性PG,进而促进胃粘膜(Na~+-K~+-Mg~(2+))-ATPase活力升高,使粘膜抵抗损伤的能力增强,可能是其保护作用的重要机制之一。
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| 关 键 词： | 适应性细胞保护 ATP酶 前列腺素 胃粘膜损伤 |
ROLE OF GASTRIC MUCOSAL Na~+--K~+--Mg~(2+)--DEPENDENT ATPase IN THE ADAPTIVE CYTOPROTECTION |
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| WANG JIAN-YING,WANG ZHI-JUN,WANG CHIH-CHUN Research Laboratory in Physiology of Digestion and Raproduction.ROLE OF GASTRIC MUCOSAL Na~+--K~+--Mg~(2+)--DEPENDENT ATPase IN THE ADAPTIVE CYTOPROTECTION[J].Acta Physiologica Sinica,1988,40(3):215-222. |
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| Authors: | WANG JIAN-YING WANG ZHI-JUN WANG CHIH-CHUN Research Laboratory in Physiology of Digestion and Raproduction |
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| Institution: | WANG JIAN-YING,WANG ZHI-JUN,WANG CHIH-CHUN Research Laboratory in Physiology of Digestion and Raproduction,Institute of Basic Medical Sciences,Beijing Medical University |
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| Abstract: | The purpose of this study was to observe the role of mucosal Na~+-K~+-Mg~(2+)dependent ATPase in the adaptive cytoprotection and its relation to endogenousprostaglandins in the rat's stomach. It was shown that ouabain, an antagonistof Na~+-K-~+ Mg~(2+)-dependent ATPase activity, partly abolished the adaptive cytopro-tection produced by pepsin 150 U in 0.1 mol/L HCI and 20% ethanol in a dosedependent manner. The gastric mucosal Na~+-K~+-Mg~(2+)-dependent ATPaseactivity was dose-dependently increased 15 min after gastric administration ofHCI and ethanol. This increase was inhibited by indomethacin. ExogenousPGE_2 restored the increase of gastric mucosal Na~+-K~+-Mg~(2+)-dependent ATPaseactivity abolished by indomethacin. These results indicate that the mild irritantscould protect gastric mucosa aganist necrosis, at least partly through the increaseof mucosal Na~+ - K~+ -Mg~(2+) -dependent ATPase activity mediated by endogenousprostoglandins formed. |
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| Keywords: | adaptive cytoprotection Na~+-K~+-Mg~(2+)-dependent ATPase prostaglandins gastric lesions |
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