目的 探讨整合素Mac-1基因缺失对自发肠道腺瘤小鼠ApcMin/+脂代谢的影响.方法 ApcMin/+小鼠和Mac-1基因缺失小鼠(Mac-1-/-)扩群获得实验所需数量小鼠,并进行杂交剪尾提取DNA,用PCR法检测小鼠基因型;计数肠道腺瘤数目和体积,并检测血清中总胆固醇(TC)和三酰甘油(TG)的变化.结果 获得Mac-1缺失的自发腺瘤ApcMin/+;Mac-1-/-小鼠.Mac-1基因缺失后,ApcMin/+小鼠小肠腺瘤数目和体积减少,血清中TC和TG均下调约40%.结论 Mac-1基因缺失抑制ApcMin/+小鼠小肠腺瘤生长可能与脂代谢有关.
Objective To investigate the influence of Mac-1 deficiency on tumor growth and lipid metabolism of spontaneous intestinal adenoma.Methods The ApcMin/+ mice and Mac-1 knock-out (Mac-1-/-) mice were expanded.The ApcMin/+ mice were mated with Mac-1-/-mice.The DNA was extracted and genotyped by PCR assay.The tumor number and volume were assessed, and the serum total cholesterol (TC) and triglyceride (TG) were detected.Results The Mac-1 deficiency mice with spontaneous intestinal adenoma were obtained.The tumor number and volume in small intestine were reduced.The serum TG and TC were both reduced by about 40%.Conclusion Mac-1 gene deletion could significantly suppress intestinal adenoma growth, that may correlate with lipid metabolism.