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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 observe the effects of Weilean on experimental rats TXL2, PGI2 and COX-2, and to explore its mechanism. Methods Forty-eight SD rats were randomly divided into normal control group, model group, Weile San low dose group, Weile San medium dose group, Weilean high dose group and ranitidine group. The rat model of gastric ulcer was prepared by cauterization with glacial acetic acid, and the rats were sacrificed on the 14th day after the continuous administration. The tissues were taken from the ulcer to extract the protein. The levels of TXB2 and 6-Keto-PGF1α in the tissue were detected by ELISA, and the ratio of TXB2 / 6-Keto-PGF1α was observed. Western blot detection of tissue COX-2 content. Results Compared with the normal control group, the levels of 6-Keto-PGF1α and COX-2 in the model group were significantly decreased (P <0.05) and TXB2 and TXB2 / 6-Keto-PGF1α were increased -Keto-PGF1α was higher than that of the normal control group (P <0.05). Compared with the model group, the content of 6-Keto-PGF1α and COX-2 in Weilean middle-high dose group and ranitidine group increased especially in the high-dose Weileosan group (P <0.01) TXB2 / 6-Keto-PGF1α was significantly lower in high-dose Weilei powder group and ranitidine group than that in model group (P <0.05) (P <0.01). Conclusion Weile powder treatment of gastric ulcer may be through the promotion of PGI2 secretion, to correct the imbalance of TXA2 / PGI2 to achieve.