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作 者:刘玮[1] 胡焕明[1] 潮欣宜[1] 金灿灿[1] 赵维中[2]
机构地区:[1]淮北职业技术学院药理学教研究,安徽淮北235000 [2]安徽医科大学药理学教研室,安徽合肥230032
出 处:《中成药》2006年第10期1473-1475,共3页Chinese Traditional Patent Medicine
基 金:安徽省教育厅课题NO:2005KJ394ZC
摘 要:目的:观察金葵胃药(JK)对胃粘膜损伤的保护作用,并探讨其机制。方法:采用阿司匹林灌胃致大鼠胃黏膜损伤模型,观察JK用药组和对照组胃黏膜损伤指数,并测定血清和胃组织中一氧化氮(NO)含量和一氧化氮合酶(NOS)活性,测定血浆中6-酮-前列腺素F1α(6-keto-PGF1α)、血栓素B2(TXB2)和血清中表皮生长因子(EGF)含量。结果:JK用药组的胃黏膜损伤指数较模型对照组显著下降,血清和胃组织中NO含量和NOS活性显著升高,血浆6-keto-PGF1α、TXB2含量和血清EGF含量明显升高。结论:JK对实验性胃黏膜损伤具有保护作用,其机制可能与增高胃黏膜保护因子有关。AIM: To investigate the protective effects and its mechanism of Jinkui Gastric Drug(JK). METHODS: The model of gastric mucosal lesion in rats induced by hydrochloride acid-aspirin was used. The indexes of gastric mucosal lesion in JK and control groups were observed. The contents of nitric oxide (NO) and the activity of nitric oxide synthase (NOS) in blood serum and gastric tissue in rats, the levels of 6-keto-PGF1α, thromboxane B2 (TXB2 ) in blood plasma and epidermal growth factor (EGF) in blood serum were examined. RESULTS: The index of gastric mucosal lesion after administration of JK reduced obviously. The contents of NO and the activity of NOS in serum and gastric tissue increased markedly. The levels of 6-keto-PGF1α, TXB2 and EGF increased significantly. CONCLUSION: JK can protect experimental gastric mucosal lesion and its mechanism may be related to increasing the protective factors.
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