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目的:观察以终末脱氧核糖核酸转移酶介导的原位缺口末端标记(terminal deoxynucleotidyl transferase-me-diated dUTP nick end labeling,TUNEL)技术检测复方蜥蜴散治疗后对CAG大鼠模型胃黏膜细胞凋亡的影响。方法:将90只SD雄性大鼠随机分为正常组,模型组,复方蜥蜴散大、中、小剂量组及维酶素组。除正常组以外,均采取55℃热盐水、2%水杨酸、20mmol/L脱氧胆酸钠3个致萎缩因素配合饥饱失常造成大鼠CAG模型,分别运用复方蜥蜴散大、中、小剂量及维酶素治疗,记录各组大鼠体重变化,以TUNEL法测定各组大鼠胃黏膜细胞凋亡率。结果:造模后大鼠体重增加缓慢,与正常组大鼠相比体重明显减轻(P<0.01)。治疗4周后,复方蜥蜴散大剂量组较模型组体重略有增加(P<0.05)。与正常组相比,模型组凋亡细胞指数显著升高(P<0.01);与模型组相比,各治疗组胃黏膜细胞凋亡率显著升高(P<0.01);与维酶素组相比,复方蜥蜴散治疗各组胃黏膜细胞凋亡率显著升高(P<0.05);与复方蜥蜴散小剂量组比较,复方蜥蜴散大剂量组胃黏膜细胞凋亡率显著升高(P<0.01)。结论:复方蜥蜴散治疗后可使CAG模型大鼠体重增加,并且可促进胃黏膜病变细胞凋亡,阻断CAG病变细胞的增殖,从而逆转胃黏膜组织萎缩,防止CAG的发生。
Objective: To observe the apoptosis of gastric mucosa in CAG rat model treated with compound lizards by terminal deoxynucleotidyl transferase-me-dia d nick end labeling (TUNEL) The impact of death. Methods: 90 male Sprague-Dawley rats were randomly divided into normal group, model group, compound lizards scattered large, medium and low dose groups and Verapamil group. In addition to the normal group were taken 55 ℃ hot salt water, 2% salicylic acid, 20mmol / L sodium deoxycholate caused by three shrinking factors with starvation caused by rat CAG model, respectively, the use of compound lizards scattered large, medium and small Dose and vitamin enzyme treatment, body weight changes were recorded in each group, the gastric mucosal cell apoptosis rate was determined by TUNEL method. Results: The rats’ body weight increased slowly after modeling, and the body weight was significantly reduced compared with the normal rats (P <0.01). After 4 weeks of treatment, the body weight of compound lizards powder group increased slightly (P <0.05). Compared with the normal group, the apoptotic index of the model group was significantly increased (P <0.01); compared with the model group, the apoptosis rate of gastric mucosal cells in each treatment group was significantly increased (P <0.01) (P <0.05). Compared with the compound lizards scattered small dose group, the apoptosis rate of gastric mucosal cells increased significantly (P <0.01). Conclusion: The treatment of compound lizards can increase the body weight of rats with CAG and promote the apoptosis of gastric mucosal lesions, block the proliferation of CAG cells, and thus reverse the atrophy of gastric mucosa and prevent the occurrence of CAG.