共轭亚油酸抑制苯并(a)芘诱导小鼠前胃癌的研究

目的：探讨不同的构成的共轭亚油酸（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-CAL组、98％纯度c9,t11-CAL组、98％纯度t10,c12-CLA组的前胃肿瘤发生率分别为100．0％、75．0％、69．2％、53．8％；蛋白印迹法分析结果表明，CAL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CAL对B(a)P诱导小鼠前胃癌均具有抑制作用；CAL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。

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

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.