小鼠前胃癌前病变阻断实验及分子学机制的变化

目的　维甲酸阻断小鼠前胃癌前病变模型 ,观察表皮生长因子受体 (EGFR)、细胞周期素D(CyclinD1)、血管内皮生长因子 (VEGF)在小鼠前胃癌变阻断前后的变化规律。方法　将 10 0只ICR雌性小鼠随机分为 3组 :A组(40只 )用诱癌剂诱导 ;B组 (40只 )在第 6周停用诱癌剂后继续灌喂维甲酸 ;C组 (2 0只 )仅服用等量的生理盐水。实验第 77天将小鼠全部处死 ,取前胃组织切片 ,免疫组化染色。结果　B组癌前病变发生率及癌总发生率均较A组明显降低。EGFR、CyclinD1、VEGF在癌变上皮的表达与组织学分级有关。A、B两组EGFR、CyclinD1、VEGF在癌前病变中表达强度与组别无关。VEGF的表达强度随着EGFR的增加而增强 ,而CyClinD1与EGFR、VEGF表达强度无关。结论　EGFR、CyClinD1、VEGF与癌肿的发生密切相关 ,而表达程度与组织学分级关系不大。在癌变过程中EGFR和VEGF有协同作用。维甲酸可降低VEGF的表达水平 ,对小鼠前胃癌前病变有明显的阻断作用。

Block of forestomach precancerous lesion in mice and changes of molecular mechanism

Objective To establish a model of blocking forestomach precancerous lesion in mice with retinoic acid and observe change patterns of EGFR, CyclinD1, and VEGF protein in forestomach precancerous lesion. Methods One hundred ICR female mice were randomly divided into three groups: Group A (40 mice) treated with simple inducing carcinoma; Group B (40 mice) which stopped being fed with carcinogen and continued to be fed with retinoic acid after 6 weeks; Group C (20 mice) merely fed with equivalence saline. All the mice were put to death on day 77, and their forestomach constitutions were made into sections by immunohistochemistrial staining. Results Incidence of precancerous lesion and total incidence of carcinoma decreased more significantly in group B than in group A. Expression of EGFR, CyclinD 1 and VEGF in carcinomatous epithelial change were associated with histological classification. Expression strength of EGFR, CyclinD 1 and VEGF in precancerous lesion in group A had nothing to do with group B. Expression of VEGF strengthened as expression strength of EGFR increased, but expression strength of CyclinD 1 had nothing to do with EGFR or VEGF. Conclusion EGFR, CyclinD 1, and VEGF have close correlation with occurrenc of carcinoma, but the degree of expression has less correlation with histological classification. EGFR and VEGF have synergistic action in occurrence and progress of the lesion. Retinoic acid may decrease level of VEGF expression, and plays an obvious role in blocking forestomach precancerous lesion in mice.