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作 者:文国容[1] 徐靖宇[1] 刘雪梅[1] 赵正兰[1] 江义霞[1] 谢睿[1] 陈萍[1] 余丽梅[2] 庹必光[1]
机构地区:[1]遵义医学院附属医院,贵州遵义563000 [2]遵义医学院贵州省细胞工程重点实验室
出 处:《山东医药》2012年第16期4-6,共3页Shandong Medical Journal
基 金:国家自然科学基金资助项目(A-030);贵州省中医药管理局[黔中医药发(2009)79号]
摘 要:目的观察胃乐散对大鼠实验性溃疡血栓素A2(TXA2)和前列腺素I2(PGI2)及环氧合酶2(COX-2)的影响,并探讨其作用机理。方法 SD大鼠48只,随机分为正常对照组、模型组、胃乐散低剂量组、胃乐散中剂量组、胃乐散高剂量组和雷尼替丁组。采用冰醋酸烧灼法制备大鼠胃溃疡模型,连续用药后第14天处死大鼠,取溃疡部位组织提取蛋白。用ELISA法检测组织中血栓素B2(TXB2)和6-酮-前列腺素F1α(6-Keto-PGF1α)的水平变化,并观察TXB2/6-Keto-PGF1α的比值变化。Western blot检测组织中COX-2的含量。结果与正常对照组比较,模型组6-Keto-PGF1α、COX-2水平降低(P<0.05),TXB2及TXB2/6-Keto-PGF1α升高(P<0.05);胃乐散高剂量组6-Keto-PGF1α的含量高于正常对照组(P<0.05)。与模型组比较,胃乐散中、高剂量组及雷尼替丁组6-Keto-PGF1α、COX-2的含量增加,特别是胃乐散高剂量组增加更为明显(P<0.01),胃乐散高剂量组及雷尼替丁组TXB2低于模型组(P<0.05),特别是TXB2/6-Keto-PGF1α降低更为显著(P<0.01)。结论胃乐散治疗胃溃疡可能是通过促进PGI2分泌,纠正TXA2/PGI2的失衡来实现的。Objective To investigate the effects of wei-le-san on thromboxane A2 ( TXA2 ), prostaglandin 12 ( PGI2 ) and cyclooxygenase-2 (COX-2) in gastric ulcers of rats, and probe its functional mechanism. Methods Forty-eight rats were randomly divided into normal group, model group, low dose of wei-le-san group, middle dose of wei-le-san group, high dose of wei-le-san group and ranitidine group. The rats of gastric ulcer were induced by glacial aceticacid. After drug treatment for 14 days, the rats gastric mucosa were collected to check the contents of TXB2 and 6-Keto-PGF1a with ELISA, COX-2 by Western blot. Results Compared with control group, the levels of 6-Keto-PGF1a, COX-2 in model group were lower ( P 〈0. 05 ), the contents of TXB2, TXB2/6-Keto-PGF1a, were higher ( P 〈 0.05 ), and wei-le-san elevated the level of 6-Keto-PGF1a, in the rats gastric mucosa. Compared to the model group, the levels of 6-Keto-PGF1a, COX-2 in middle dose of wei-le-san group, high dose of wei-le-san group and ranitidine group increased (P 〈 0.05 ), and the contents of TXB2, TXB2/6-Keto-PGF1a decreased (P 〈 0.05). Conclusion Increasing the level of PGI2 and correcting the unbalance of TXA2/PGI2 may be one of the possible mechanisms of wei-le-san to cure gastric ulcer.
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