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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。
Objective: To investigate the effect of FFXY treatment on the expression of apoptosis-related protein IKKβ and vascular endothelial growth factor (VEGF) in gastric cancer precancerous lesions (PLGC), and to explore its possible mechanism of action in treating PLGC. Methods: One hundred and twenty Sprague-Dawley rats were randomly divided into 6 groups. All the treatment groups were treated with MNNG combined with starvation insufficiency and emotional stimulation synthesis, and blank control group Normal supply of standard feed and clean distilled water. The rats were treated respectively after successful modeling. The expression of IKKβ and VEGF in gastric mucosa was detected by immunohistochemistry, and the statistical analysis of the experimental results was carried out. Results: The expressions of IKKβ and VEGF in model group were higher than those in blank control group (P <0.01). The expression of IKKβ and VEGF in model group was lower than that in model control group (P <0.05) (P <0.05). The positive expression of the two factors in 80-mesh and 100-mesh mixed groups was lower than that in 80-mesh and 100-mesh groups (P <0.05). CONCLUSION: FFXY is effective in treating PLGC in each group, and in the FFXY group, the effect of FFXY in PLGC rats is better than that in vitamin E group, especially in the 80-mesh 100-mesh mixed dose group. These results suggest that the compound lizards may have protective and repair effects on gastric mucosal injury. The mechanism may be through decreasing or inhibiting the expression of IKKβ and VEGF in PLGC tissues, promoting apoptosis and inhibiting angiogenesis.