化浊解毒和胃方对胃癌前病变大鼠血管生成机制的影响

目的探讨化浊解毒和胃方治疗胃癌前病变（precancerous lesions of gastric cancer， PLGC）在血管新生方面的可能机制。方法Wistar大鼠66只随机分为6组：即正常对照组（空白组），模型组，维甲酸治疗组（维甲酸组），化浊解毒和胃方高、中、低剂量治疗组，每组11只。采用幽门弹簧插入复合法复制慢性萎缩性胃炎PLGC模型，各组给予相应的药物每天灌胃1次，每次2 mL，连续12周。采用免疫组织化学和Western blot方法，观察化浊解毒和胃方对慢性萎缩性胃炎PLGC大鼠胃黏膜组织缺氧诱导因子－1α（hypoxia induced factor，HIF-1α）、血管内皮生长因子（vascular endothelial growth factor，VEGF）的影响。结果与空白组比较，模型组VEGF、HIF-1α的表达增高，差异有统计学意义（P<0.05）；各治疗组与模型组比较，VEGF、HIF-1α表达降低，差异有统计学意义（P<0.05）；且化浊解毒和胃方高剂量组与中剂量组降低VEGF、HIF-1α的表达优于维甲酸组及化浊解毒和胃方低剂量组（P<0.05），低剂量组与维甲酸组比较差异无统计学意义（P>0.05）。结论化浊解毒和胃方可能是通过降低PLGC大鼠胃黏膜HIF-1α、VEGF的表达，从而抗血管生成达到防治慢性萎缩性胃炎PLGC的治疗效果，并且存在一定的量效关系。

英文摘要:

ObjectiveTo explore the possible angiogenesis mechanism of Huazhuo Jiedu Hewei Recipe （HJHR） in preventing and treating precancerous lesions of gastric cancer （PLGC）. MethodsTotally 66 Wistar rats were randomly divided into 6 groups， i.e.， the normal control group， the model group， the retinoic acid （RA） group， the high dose HJHR group， the middle dose HJHR group， the low dose HJHR group， 11 in each group. PLGC model was duplicated by inserting a spring with Helicobacter. Corresponding medicines were administered to rats in each medicated group once daily by gastrogavage， 2 mL each time for 12 successive weeks. The effect of HJHR on hypoxia induced factor （HIF-1α） and vascular endothelial growth factor （VEGF） of PLGC in chronic atrophic gastritis （CAG） rats′ gastric mucosa was observed by immunohistochemical assay and Western blot method. ResultsCompared with the normal control group， the expression of VEGF and HIF-1α increased in the model group （P<0.05）. Compared with the model group， the expression of VEGF and HIF-1α decreased in each medicated group （P<0.05）. Besides， they were lower in the high and middle dose HJHR groups than in the RA group and the low dose HJHR group （P<0.05）. There was no statistical difference between the low dose HJHR group and the RA group （P>0.05）. ConclusionHJHR could prevent and treat PLGC of CAG rats possibly through decreasing the expression of HIF-1α and VEGF in a dose-dependent manner.

关闭