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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。
In this paper, we observed the role of gastric mucosa (Na ~ + -K ~ + -Mg ~ (2 +)) - ATPase in adaptive cytoprotection and analyzed its relationship with endogenous PG. The results showed that ouabain, an inhibitor of Na ~ + -K ~ + -Mg ~ (2 +) - ATPase, could partially inhibit pepsin 150U (dissolved in 0.1mol / L hydrochloric acid) and 20% Ethanol adaptive cytoprotection, and showed a significant dose-response relationship. The gastric mucosa (Na ~ + -K ~ + -Mg ~ (2 +)) - ATPase activity was significantly increased 15 minutes after the above two kinds of weak stimulation, also showed a significant dose-effect relationship. Pretreatment with indomethacin to inhibit the synthesis of endogenous PG blocked the increase in the activity of gastric mucosa (Na ~ + -K ~ + -Mg ~ (2 +)) - ATPase induced by weak stimulation; On the basis of giving exogenous PGE 2, but also lifted the blocking effect of indomethacin. These results indicate that the weak stimulation through the endogenous PG, and then promote the gastric mucosa (Na ~ + -K ~ + -Mg ~ (2 +)) - ATPase activity increased, the ability of the mucosa to resist damage increased, may be its protection One of the important mechanisms of action.