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Investigation on the mechanisms involved in the central protective effect of amylin on gastric ulcers in rats

机译:胰岛淀粉样多肽对大鼠胃溃疡中枢保护作用机制的研究

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The mechanisms involved in the protective effect of amylin (administered into the brain ventricle, i.c.v.) on gastric ulcers induced by the oral administration of ethanol 50/100(EtOH), 1 ml/rat) or indomethacin (indomethacin, 20 mg kg~-1, at a dosing volume of 5 ml) were investigated in rats. The possible involvement of endogenous nitric oxide (NO) in the beneficial effect of amylin against EtOH-induced ulcers was examined. The inhibitor of NO-synthesis, N~G-nitro-L-arginine methyl ester (L-NAME, 70 mg kg~-1, s.c.) was injected 30 min before amylin (2.2 μg/rat, i.c.v.) followed by EtOH after a further 30 min. Rats were sacrified 1 h after EtOH. L-NAME completely removed the protective effect of amylin.
机译:胰岛淀粉样多肽(施用于脑室,ICV)对口服乙醇(50/100(乙醇),1 ml /大鼠)或消炎痛(吲哚美辛,20 mg kg〜-)诱导的胃溃疡的保护机制如图1所示,在大鼠中以5ml的剂量体积进行了研究。检查了内源性一氧化氮(NO)可能参与了胰岛淀粉样多肽对EtOH诱导的溃疡的有益作用。 NO合成抑制剂N〜G-硝基-L-精氨酸甲酯(L-NAME,70 mg kg〜-1,sc)在胰岛淀粉样多肽(2.2μg/ rat,icv)前30分钟注射,随后在注射EtOH之后再过30分钟。 EtOH 1 h后处死大鼠。 L-NAME完全消除了胰岛淀粉样多肽的保护作用。

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