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为探讨维生素D3促进大鼠胃癌血管新生的机制 ,取Wistar大鼠 12只作为空白对照 (Ⅰ组 ) ,饲常规饲料 ;另将 12 0只经饮水摄入N 甲基 N′ 亚硝基 N 亚硝基胍 (MNNG ,15 0mg/L) 4周制作大鼠胃癌模型 ,之后均分为 3组 :Ⅱ组为对照 (MNNG) ,饲常规饲料 ;Ⅲ、Ⅳ组分别饲以 1,2 5 二羟基维生素D3[1,2 5 (OH) 2 D3]添加饲料(2 .5 μg/kg和 5 .0 μg/kg)。于实验 16、32周处死动物 ,处死前行活体心血管内墨汁灌注。进行血管内皮细胞生长因子 (VEGF)免疫组织化学染色和微血管密度测定。结果显示 ,实验 16周Ⅳ组VEGF表达和微血管密度明显高于MNNG组 (P <0 .0 5 ) ,至实验 32周达到更为显著水平 (P <0 .0 1) ;VEGF表达与微血管密度密切相关 (r =0 6 0 4,P <0 .0 1)。提示VEGF表达增强可能是 1,2 5 (OH) 2 D3促进大鼠胃癌血管新生的机制之一。
To explore the mechanism of vitamin D3 in promoting gastric cancer angiogenesis in rats, 12 Wistar rats were used as blank control (group I) and fed conventional diet; another 120 rats were ingested with N methyl-N-nitroso-N Nitroguanidine (MNNG, 150 mg/L) was used to make rat gastric cancer models for 4 weeks, and then divided into 3 groups: Group II as control (MNNG) and conventional feed; Group III and IV were fed with 1,25 Hydroxyvitamin D3 [1,25 (OH) 2 D3] was added to feed (2.5 μg/kg and 5.0 μg/kg). Animals were sacrificed 16 and 32 weeks after the experiment, and intravital intravascular ink infusion was performed before sacrifice. Vascular endothelial growth factor (VEGF) immunohistochemical staining and microvessel density measurements were performed. The results showed that the VEGF expression and microvessel density in group IV were significantly higher than those in MNNG group (P < 0.05) at week 16 and reached a more significant level at 32 weeks (P < 0.01); VEGF expression and microvessel density Closely related (r = 606.4, P < 0.01). This suggests that the enhanced expression of VEGF may be one of the mechanisms by which 1.25 (OH) 2 D3 promotes angiogenesis in rat gastric cancer.