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目的:研究胃炎Ⅰ号对CAG大鼠胃黏膜基质金属蛋白酶-1(MMP-1)和基质金属蛋白酶抑制因子-1(TIMP-1)酶活性的影响,探讨胃炎Ⅰ号对CAG大鼠胃黏膜损伤的疗效作用机制。方法:采用胃炎I号煎剂高中低剂量浓度及维酶素治疗慢性萎缩性胃炎大鼠模型,明胶酶谱法检测MMP-1酶活性,反向明胶酶谱法测TIMP-1酶活性。结果:模型大鼠胃黏膜组织MMP-1酶活性明显升高(P<0.01);经中剂量胃炎I号治疗后,病变大鼠胃黏膜MMP-1酶活性水平下降(P<0.01),基本接近正常水平(P>0.01)。模型大鼠胃黏膜TIMP-1酶活性低于空白对照组(P<0.01)。经高、中剂量胃炎I号和西药对照治疗后大鼠胃黏膜TIMP-1酶活性升高(P<0.01),中剂量胃炎I号治疗后TIMP-1酶活性基本接近空白对照组水平(P>0.05),疗效最佳。结论:在慢性萎缩性胃炎阶段,MMP-1酶活性升高,TIMP-1酶活性降低。降低MMP-1酶活性,提高TIMP-1酶活性,可能是胃炎I号治疗慢性萎缩性胃炎的作用机制之一。
Objective: To investigate the effect of Weiyan I on the activity of matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-1 (TIMP-1) in gastric mucosa of CAG rats and the effect of Weiyan I on gastric mucosa Efficacy of injury mechanism of action. Methods: The model of chronic atrophic gastritis was treated by high and low dose of Weiyan I decoction and the treatment of chronic atrophic gastritis with gemcitabine. The activity of MMP-1 was detected by gelatin zymography and the activity of TIMP-1 by reverse gelatin zymography. Results: The activity of MMP-1 in gastric mucosa was significantly increased in model rats (P <0.01). The activity of MMP-1 in gastric mucosa of rats with moderate-dose gastritis was decreased (P <0.01) Close to the normal level (P> 0.01). The activity of TIMP-1 in gastric mucosa in model rats was lower than that in control group (P <0.01). The activity of TIMP-1 in gastric mucosa of rats after high-dose and middle-dose gastritis I and western medicine treatment increased (P <0.01), while the activity of TIMP-1 in medium dose gastritis I was almost the same as that of the blank control group (P > 0.05), the best effect. Conclusion: In the chronic atrophic gastritis stage, the activity of MMP-1 increases and the activity of TIMP-1 decreases. Reducing the activity of MMP-1 and increasing the activity of TIMP-1 may be one of the mechanisms of gastritis I in treating chronic atrophic gastritis.