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半夏泻心汤对大鼠乙酸型胃溃疡的保护作用

Protective effect of Banxiaxiexin decoction on the experimental rats with gastric ulcer caused by acetic acid

    摘要
  • 摘要:
    目的 探讨半夏泻心汤对大鼠乙酸型胃溃疡的治疗作用及机制。
    方法 将48只实验大鼠随机分为6组：正常组，模型对照组，半夏泻心汤低、中、高剂量组，奥美拉唑组，每组8只。采用改良Okabe法制备慢性乙酸胃溃疡模型。造模后，模型对照组每次给予生理盐水4 mL灌胃，2次/d；半夏泻心汤低、中、高剂量组每次分别给予半夏泻心汤灌胃，给药剂量分别为1、2、4 mL/kg，2次/d；奥美拉唑组每次给予奥美拉唑溶液4 mL灌胃，给药剂量为0.36 g/kg，1次/d，连续14 d。在连续给药14 d后，于第15天处死大鼠，收集大鼠的溃疡基底和正常胃组织标本，测定大鼠溃疡指数、溃疡抑制率和胃酸pH值，血清i-NOS、t-NOS、NO和溃疡组织中内皮生长因子（VEGF）蛋白的表达。
    结果 半夏泻心汤低、中、高剂量组溃疡指数低于模型对照组，溃疡抑制率高于模型对照组，差异有统计学意义（P < 0.05），且其中半夏泻心汤高剂量组溃疡抑制率较模型组改善最为明显。与模型对照组比较，半夏泻心汤低、中、高剂量组能升高胃酸pH值，增加血清t-NOS和NO的表达，降低血清i-NOS的表达，差异有统计学意义（P < 0.05）。与模型对照组相比，半夏泻心汤低、中、高剂量组促进溃疡基底部组织VEGF的表达，差异有统计学意义（P < 0.05）。
    结论 半夏泻心汤对大鼠乙酸型胃溃疡有治疗作用，其通过升高胃酸pH值，增强t-NOS、NO和VEGF的表达，降低i-NOS的表达发挥作用。

     

    Abstract:
    Objective To explore the effects and mechanism of Banxiaxiexin decoction (BXD) on experimental gastric ulcer in rats.
    Methods Forty-eight rats were randomly divided into six groups: normal, control, Omeprazole treatment, low-dose, mid-dose, and high-dose of BXD treatment groups with 8 in each group. Models were established using the improved Okabe method. After modeling, rats in the control group were given 4 mL of normal saline twice a day. Low-dose, mid-dose, and high-dose BXD were administered twice a day by gavage at the dosage of 1, 2, and 4 mL/kg, respectively. Omeprazole (4 mL) was given to models daily at the dosage of 0.36 g/kg. After having been given BXD for 14 days, all groups of rats were sacrificed on the 15th day, the normal gastric condition and the gastric ulcer tissue were examined. Gastric ulcer tissue was evaluated by ulcer index (UI), ulcer inhibition rate, pH of gastric acid, i-NOS, t-NOS, NO in serum, and the expression of VEGF in the ulcer tissue.
    Results Compared with the control group, UI in the low/middle/high-dose of BXD group was lower than that in the control group. Ulcer inhibition rate in the low group was higher than that in the model group, the differences were all statistically different (P < 0.05), and the ulcer inhibition rate of the high-dose group (P < 0.01) was significantly improved than that of the model group when compared with other groups. Moreover, pH of gastric acid, t-NOS, and NO in serum were increased in BXD groups (P < 0.05) especially in high dose group (P < 0.01) when compared with the model group, while i-NOS in serum was declined, the differences were all statistically different. Compared with the model group, VEGF expressed in gastric ulcer tissue in the low-, medium-, and high-dose of BXD group were promoted, the differences were all statistically different (P < 0.05).
    Conclusions BXD can significantly promote gastric ulcer healing and its mechanism may be related to the rise of pH of gastric acid, t-NOS, NO in serum and VEGF expressed in gastric ulcer tissue and the decline of i-NOS in serum.

     

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