目的 探讨去氢吴茱萸碱对实验性胃溃疡大鼠胃黏膜的保护作用及机制，为临床应用提供数据。方法 选取雄性健康SD大鼠，采用乙酸烧灼法建立胃溃疡模型。将40只模型大鼠随机分为模型组，去氢吴茱萸碱低、高（6.25、12.5 mg/kg）剂量组和阳性对照（奥美拉唑10 mg/kg）组，另取10只健康大鼠设为假手术组。各组大鼠ig相应剂量药物，假手术组与模型组大鼠则给予等量生理盐水。14 d后，比较各组大鼠的胃溃疡面积、胃溃疡抑制率、胃黏膜修复因子、血清氧化应激因子、血清炎症因子、胃组织相关蛋白水平。结果 与模型组比较，去氢吴茱萸碱可显著降低胃黏膜溃疡面积（P<0.05、0.01），显著升高胃溃疡抑制率；可有效促进胃组织中三叶因子1（TFF1）和胃组织表皮生长因子（EGF）水平的增加（P<0.05、0.01）；可明显降低大鼠血清中丙二醛（MDA）、环氧酶2（COX-2）、肿瘤坏死因子（TNF-α）和白细胞介素（IL-6）水平；明显提高血清中谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）活性（P<0.05、0.01）；同时大幅下调胃组织中Rho、ROCK1、ROCK2和NF-κB的表达水平（P<0.05、0.01）。结论 去氢吴茱萸碱可通过抗氧化应激、抗炎症因子对大鼠胃溃疡产生明显改善作用，其潜在作用机制可能与调控Rho/NF-κB信号通路有关。

Objective To investigate the protective effect and mechanism of dehydroevodiamine on gastric mucosa of rats with experimental gastric ulcer and its mechanism, so as to provide objective data for clinical application. Methods Male SD rats were selected and the gastric ulcer model was established by acetic acid cauterization. Forty model rats were randomly divided into model group, dehydroevodiamine low-dose (6.25 mg/kg) group, dehydroevodiamine high-dose (12.5 mg/kg) group, and positive control (omeprazole 10 mg/kg) group. Another 10 healthy rats were selected as the sham group. The rats in each group were ig the corresponding dose of drugs, while the rats in the sham group and the model group were given the same amount of normal saline. After the end of experiment for 14 d, the area and inhibition ratio of gastric ulcer, repair factor of gastric mucosa, serum oxidative stress factor, inflammatory factor, and gastric tissue-related protein levels were compared. Results Compared with the model group, dehydroevodiamine could decrease the area of gastric ulcer significantly (P<0.05, 0.01), and increase the inhibition ratio of gastric ulcer significantly. Dehydroevodiamine could increase the trefoil factor family 1 (TFF1) and stomach tissue epidermal growth factor (EGF) significantly (P<0.05, 0.01), and could decrease the serum malondialdehyde (MDA), cyclooxygenase 2 (COX-2), tumor necrosis factor (TNF-α) and IL-6. Dehydroevodiamine could increase the activity of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) (P<0.05, 0.01), and could decrease the expression levels of Rho, ROCK1, ROCK2 and NF-κB in gastric tissues (P<0.05, 0.01). Conclusion Dehydroevodiamine can significantly improve gastric ulcer in rats through anti-oxidative stress and anti-inflammatory factors, and its potential mechanism may be related to the regulation of Rho/NF-κB signaling pathway.

R285.52