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[目的]探讨愈疡散对胃溃疡大鼠血一氧化氮(NO)和内皮素-1(ET-1)的影响。[方法]采用大鼠冰醋酸胃溃疡模型,设空白对照组(A组)、假手术组(B组)、西药对照组(C组)、愈疡散大、小剂量组(D、E组)、胃溃疡模型组(F)。A、B、F组均灌服0.85％氯化钠溶液;D、E组分别灌服愈疡散5.0g／kg体重、2.5 g／kg体重;C组灌服雷尼替丁0.03g/kg体重。于治疗前后分别检测血NO及ET-1。实验结束后,用苏木精-伊红染色对大鼠再生胃黏膜厚度、上皮细胞／腺腔数比值进行观察。[结果]造模7 d,C、D、E、F组血清NO显著降低,血浆ET-1明显升高,与A、B组比较差异有统计学意义(P<0.05)。治疗28 d,D组血清NO显著升高,而血浆ET-1明显降低,与F、E组比较均P<0.05。再生胃黏膜厚度:D、E、C组明显高于F组(P<0.05),D、E组与A、B组比较均P<0.05。上皮细胞／腺腔数比值:A、B组与C、F组,D组与C、F组之间均P<0.05。[结论]愈疡散促进溃疡愈合,增加胃黏膜的防御能力,提高再生黏膜功能成熟度,可能与其诱导、促进NO合成,反馈性地抑制ET-1释放,维持NO和ET-1动态平衡有关。
[Objective] To explore the effect of Yuyang Powder on nitric oxide (NO) and endothelin-1 (ET-1) in gastric ulcer rats. [Method] Rat glacial acetic acid gastric ulcer model was used. The blank control group (group A), sham operation group (group B), western medicine control group (group C), Yuyangsan large and small dose group (group D and E) were used. ), gastric ulcer model group (F). Group A, B and F were given 0.85% sodium chloride solution; Groups D and E were fed with Yuyang Powder 5.0 g/kg body weight and 2.5 g/kg body weight respectively; Group C was given ranitidine 0.03 g/kg. body weight. Serum NO and ET-1 levels were measured before and after treatment. After the end of the experiment, hematoxylin-eosin staining was used to observe the regenerated gastric mucosal thickness and the ratio of epithelial cells to glandular cavities. [Results] 7 days after model establishment, serum NO in group C, D, E, F decreased significantly, plasma ET-1 increased significantly, and there was a significant difference compared with group A and B (P<0.05). After 28 days of treatment, serum NO in group D was significantly increased, while plasma ET-1 was significantly decreased, compared with group F and group E, P<0.05. Regenerated gastric mucosa thickness: D, E, C group was significantly higher than F group (P <0.05), D, E group and A, B group were P <0.05. The ratio of epithelial cells to glandular cavities: A, B group and C, F group, D group and C, F group were P <0.05. [Conclusion] Yuyang Powder can promote ulcer healing, increase the defense ability of gastric mucosa, increase the functional maturity of regenerative mucosa, may induce and promote the synthesis of NO, feedback inhibit the release of ET-1, and maintain the dynamic balance of NO and ET-1. .