中文摘要：

目的：研究复方蜥蜴散不同微粒组合剂（简称FFXY）治疗对胃癌前病变（PLGC）大鼠凋亡相关蛋白IKKβ及血管内皮生长因子（VEGF）表达的影响,揭示其治疗PLGC的可能作用机制。方法：将120只SPF级SD大鼠随机分为6组,各治疗组均采取单功能烷化剂甲基硝基亚硝基胍（MNNG）配合饥饱失常及情绪刺激综合造模,空白组正常供应标准饲料及清洁蒸馏水。造模成功后分别作相应处理,应用免疫组化法检测胃黏膜组织IKKβ、VEGF蛋白的表达,并对实验结果进行统计分析。结果：IKKβ、VEGF两种蛋白的表达情况,模型组阳性表达高于空白对照组（P〈0.01）;其他各治疗组阳性表达均低于模型对照（P〈0.05）;FFXY各治疗组阳性表达均低于维酶素治疗组（P〈0.05）;80目100目等量混合组两种因子阳性表达低于80目组和100目组（P〈0.05）。结论：FFXY各组和维酶素组治疗PLGC均有效,其中,FFXY各组对PLGC大鼠疗效均优于维酶素组,尤以80目100目等量混合剂量组疗效最显著。提示复方蜥蜴散不同微粒组合剂对胃黏膜损伤可能具有保护、修复作用,其作用机制可能是通过降低或抑制PLGC组织中IKKβ、VEGF的表达,从而促进细胞凋亡和抑制血管生成来实现的。

英文摘要：

Objective： Study the effect of different particle composition of compound lizards powder （ FFXY ） therapy on expression of IKK [3 and VEGF in PLGC model rats, reveals the possible mechanism for the treatment of PLGC. Methods： 120 SPF SD rats were randomly divided into 6 groups, the treatment group were taken MNNG with hunger disorders and emotional stimuli comprehensive building, feed and clean distilled water supply blank group standards. Building after a successful make corresponding processing respectively, using immunohistochemical method to detect gastric mucosa tissue IKK 15 , the expression of VEGF protein, and the experimental results were analyzed. Results ： IKK {5 and VEGF protein expression of model group, positive expression is higher than the blank control group （ P〈0.01 ）; positive expression of the other treatment group were lower than control group （ P〈0.01 ）; the positive expression of FFXY treatment group were lower than vatacoenayme treatment group （ P〈0.05 ）; two factor positive expression of 80 mesh 100 mesh equivalent mixing group is lower than 80 mesh and 100 mesh group （ P〈0.05 ）. Conclusion ： FFXY groups and vatacoenayme group were effective on treating PLGC, among them, the FFXY group curative effect of PLGC rats were superior than vatacoenayme group, the 80 mesh 100 mesh equivalent mixing group has the most significant curative effect especially. Different particle composition of compound lizards powder may have protection and repair effect on gastric mucosa injury, its mechanism may be through reducing or inhibiting IKK β , the expression of VEGF in PLGC organization, so as to promote apoptosis and inhibition of angiogenesis.