目的 建立用程序升温气相色谱法测定奶制品中c9，t11一共轭亚油酸含量的方法。方法 首先建立本实验方法的气相色谱分析条件；采用内标法，将样品提职、甲酯化后，进行气相色谱分析；同时对实验方法的回收率、精密度也进行了分析。结果 能够将甲酯化亚油酸和：9．tll一共轭亚油酸秘好地分离；内标物十七烷酸甲酯与其它脂肪酸甲酯能够完全分离，并不受样品中其它组分的影响；c9，tll-共轭亚油酸的含量分别为：帕玛拉特天然酸奶饮品10.78mg/g万家宝原味酸奶（搅拌型）5.03m/g．奶油22.54mg/g脂肪。实验方法的回收率为84.74%，RSD=3.73%，精密度RSD=2.58%。结论 所建立的实验条件准确可靠，这对于分析奶敏奶制品来源的c9，tll-CLA共轭亚油酸含量具有指导意义。

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100.0%、75.0%、69.2%、53.8%；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。

Objectives:To determine the effect of cis-9, trans-11-conjugated linoleic acid on the cell cycle ofmammary cancer cells (MCF-7) and its possible mechanism of inhibition cancer growth. Methods:Using cell culture and immunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, p16ink4aand p21cip/waf1of MCF-7 cells which were treatedwith various c9, t11-CLA concentrations (25mM, 50mM, 100mM and 200 M) of c9, t11-CLA for 24 and48 h, with negative controls (0.1% ethanol). Results: The cell growth and DNA ynthesis of MCF-7 cells were inhibited by c9, t11-CLA. MCF-7cells, after treatment with various c9, t11-CLA doses mentioned above for 8 days, the nhibition frequencywas 27.18%, 35.43%, 91.05%, and 92.86%, respectively and the inhibitory effect of c9,t11-CLA on DNA synthesis (except for 25mM, 24 h) incorporated significantly less3H-TdR than did the negative control(P<0.05 and P<0.01). To furtherinvestigate the influence on the cell cycle progression, we found that c9, t11-CLA may arrest the cell cycle of MCF-7 cells. Immunocytochemical staining demonstrated that MCF-7 cellspreincubated in media supplemented with different c9, t11-CLA concentrations at various times significantlydecreased the expressions of PCNA, and Cyclin A, B1, D1compared with the negative controls(P<0.01), whereas the expressions of p16ink4aand p21cip/waf1, cyclin-dependent kinases inhibitors (CDKI),were increased. Conclusions: The cell growth and proliferation of MCF-7 cellsis inhibited by c9, t11-CLA by blockingthe cell cycle, which reduces expressions of cyclin A, B1, D1and enhances expressions of CDKI (p16ink4aandp21cip/waf1).

目的 用苯并（a）芘〔B（a）P〕建立小鼠前胃癌模型，观察不同构成的共轭亚油酸（CLA）对前胃癌的抑制作用以及与脂质过氧化的关系。方法 通过灌胃方式给予昆明种小鼠B(a)p，建立前胃癌模型。用光学显微镜作病理组织检查，用比色法测定丙二醛（MDA）含量。结果 利用B(a)p 成功地在昆明种小鼠体内建立了前胃癌模型，病理结果分析表明所建立的前胃癌为鳞状细胞癌；小鼠前胃肿瘤的计数结果表明，B(a)p 组，75% c9，tll-CLA组，98% t10，c12-ClA组的肿瘤发生率分别为!100%，75.0%，69.2%和53.8%并且75%c9，t11-CLA，98%c9，98%t10，c12-CLA明显降低前胃肿瘤的直径，但对荷瘤小鼠的平均荷瘤数没有影响；与阴性对照组和B（a）P对照组相比，CLA处理能提高小鼠体内MDA含量。结论 B（a）P诱导昆明种小鼠的前胃组织形成鳞状细胞癌；不同构成CLA对B（a）P诱导小鼠前胃癌均具有抑制作用，并且MDA可能是CLA发挥预防肿瘤作用的可能机理之一。

AIM: To determine the effect of cis-9,trans-11-conjugated linoleic acid (c9, t11-CLA) on the cell cycleof gastric cancer cells(SGC-7901)and its possiblemechanism in inhibition cancer growth. METHODS: Using cell culture andimmunocytochemical techniques, we examined the cell growth, DNA synthesis, expression of PCNA, cyclin A, B1, D1, P16ink4aand p21cip/waf1 of SGC-7901 cells which were treatedwith various c9,t11-CLA concentrations (25, 50, 100 and 200μmol·L-1) of c9, t11-CLA for 24 and 48h, with anegative control (0.1% ethane). RESULTS: The cell growth and DNA synthesis of SGC-7901cells were inhibited by c9, t11-CLA. SGC-7901 cells. Eightday after treatment with various concentrations of c9, t11-CLA mentioned above, the inhibition rates were 5.92%, 20.15%, 75.61% and 82.44%,respectively andinhibitory effect of c9, t11-CLA on DNA synthesis (exceptfor 25μmol/L,24h) showed significantly less 3H-TdRincorporation than that in the negative controls (P<0.05 and P<0.01). Immunocytochemical stainingdemonstrated that SGC-7901 cells preincubated in mediasupplemented with different c9,t11-CLA concentrationsat varioustimes significantly decreased the expressionsof PCNA (the expression rates were 7.2-3.0%,24h and9.1-0.9% at 48h, respectively), Cyclin A (11.0-2.3%, 24hand 8.5-0.5%, 48h), B1 (4.8-1.8% at 24h and 5.5-0.6%at 48h) and D1 (3.6-1.4% at 24h and 3.7%-0 at 48h) ascompared with those in the negative controls(theexpressions of PCNA, Cyclin A, B1 and D1 were 6.5% at24h and 9.0% at 48h, 4.2% at 24h and 5.1% at 48h,9.5% at 24h and 6.0% at 48h, respectively) (P<0.01), whereas the expressions of p16ink4a and p21cip/waf1, cyclindependentkinases inhibitors(CDKI), were increased. CONCLUSION: The cell growth and proliferation of SGC-7901 cell is inhibited by c9,t11-CLA via blocking the cellcycle, with reduced expressions of cyclin A,B1 and D1 andenhanced expressions of CDKI(p16ink4a and p21cip/waf1).