共轭亚油酸抑制苯并(a)芘诱导小鼠前胃癌的研究  被引量:12

The inhibition of mouse forestomach neoplasm induced by B(a)P through MAPKs pathway by conjugated linoleic acid

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作  者:薛英本[1] 陈炳卿[1] 刘家仁[1] 郑玉梅[1] 刘瑞海 

机构地区:[1]黑龙江省哈尔滨医科大学公共卫生学院营养与食品卫生教研室,150001 [2]FoodScienceDepartmentofCornellUniversityUSA

出  处:《中华预防医学杂志》2001年第3期163-166,共4页Chinese Journal of Preventive Medicine

基  金:国家自然科学基金资助 (3 9870 661)

摘  要:目的 探讨不同构成的共轭亚油酸 (CLA)对苯并 (a)芘 [B(a)P]诱导的小鼠前胃癌的抑制作用及可能机制。方法 用B(a)P在昆明种小鼠体内建立前胃癌模型 ,观察不同构成的CLA对小鼠前胃癌形成的抑制作用 ,同时采用蛋白印迹法分析小鼠前胃组织中的蛋白表达情况。结果 B(a)P组、75 %纯度c9,t11 CLA组、98%纯度c9,t11 CLA组、98%纯度t10 ,c12 CLA组的前胃肿瘤发生率分别为 10 0 0 %、75 0 %、6 9 2 %、5 3 8% ;蛋白印迹法分析结果表明 ,CLA抑制ERK 1的表达 ,促进MKP 1的表达 ,而对MEK 1的表达无明显影响。结论 不同构成的CLA对B(a)P诱导小鼠前胃癌均具有抑制作用 ;CLA影响MAPKs级联反应ERKs及此途径负调控子MKP 1蛋白的表达可能是其抑制肿瘤作用的机制之一。Objective To explore the inhibition of the formation of forestomach neoplasm and its possible mechanism by conjugated linoleic acid (CLA) isomers. Methods The forestomach neoplasm model induced by B(a)P in Kunming mouse was established The numbers of tumor in forestomach were counted and the expression of MEK 1,ERK 1 and MKP 1 protein in forestomach neoplasm was studied by Western Blotting assay. Results The incidence of neoplasm in B(a)P group (positive control),75% purity c9,t11 CLA group,98% purity c9,t11 CLA group,and 98% purity t10,c12 CLA group was 100.0%,75 0%,69 2%,and 53 8%,respectively It was also found that CLA inhibited the expression of ERK 1 protein and promote the expression of MKP 1 protein,however no influence of CLA on MEK 1 protein was observed in this study. Conclusions The inhibitory effects of different isomers of conjugated linoleic acid on the formation of forestomach neoplasm in mice was significant and the effect of CLA on the expression of ERK 1 and MKP 1 may be one of the mechanisms of the inhibition of CLA on mouse forestomach tumor formation.

关 键 词:共轭亚油酸 胃肿瘤 有丝分裂原激活蛋白激酶类 癌前状态 苯并(A)芘 

分 类 号:R735.2[医药卫生—肿瘤]

 

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