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首页> 外文期刊>World Journal of Gastroenterology >Inhibition of conjugated linoleic acid on mouse forestomach neoplasia induced by benzo (a) pyrene and chemopreventive mechanisms
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Inhibition of conjugated linoleic acid on mouse forestomach neoplasia induced by benzo (a) pyrene and chemopreventive mechanisms

机译：共轭亚油酸对苯并（a）pyr诱导的小鼠前胃肉瘤形成的抑制作用和化学预防机制

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摘要

AIM: To explore the inhibition of conjugated linoleic acid isomers in different purity (75% purity c9, t11-, 98% purity c9, t11- and 98% purity t10,c12-CLA) on the formation of forestomach neoplasm and cheopreventive mechanisms. METHODS: Forestomach neoplasm model induced by B(a) P in KunMing mice was established. The numbers of tumor and diameter of each tumor in forestomach were counted; the mice plasma malondialdehyde (MDA) were measured by TBARS assay; TUNEL assay was used to analyze the apoptosis in forestomach neoplasia and the expression of MEK-1, ERK-1, MKP-1 protein in forestomach neoplasm were studied by Western Blotting assay. RESULTS: The incidence of neoplasm in B(a)P group, 75% purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity t10, C12-CLA group was 100%, 75.0% P>0.05), 69.2% (P<0.05) and 53.8% (P<0.05) respectively and the effect of two CLA isomers in 98% purity on forestomach neoplasia was significant; CLA showed no influence on the average tumor numbers in tumor-bearing mouse, but significantly decreased the tumor size, the tumor average diameter of mice in 75% purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity t10, c12-CLA group was 0.157+-0.047 cm, 0.127+-0.038 cm and 0.128+-0.077cm (P<0.05) and 0.216+-0.088 cm in B(a)P group; CLA could also significantly increase the apoptosis cell numbers by 144.00+-20.31, 153.75+-23.25, 157.25+-15.95 (P<0.05) in 75 % purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity tlO,c12-CLA group (30.88+-3.72 in BP group); but there were no significant differences between the effects of 75% purity c9, t11-CLA and two isomers in 98% purity on tumor size and apoptotic cell numbers; the plasma levels of MDA in were increased by 75% purity c9, t11-CLA, 98% purity c9, t11-CLA and 98% purity t10, c12-CLA. The 75% purity c9, t11-CLA showed stronger inhibition; CLA could also inhibit 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. CONCLUSION: Two isomers in 98% purity show stronger inhibition on carcinogenesis. However, the inhibitory mechanisms of CLA on carcinogenesis is complicated, which may be due to the increased mice plasma MDA, the inducing apoptosis in tumor tissues. 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 the tumor.
机译：目的：探讨不同纯度（75％纯度的c9，t11-，98％纯度的c9，t11-和98％纯度的t10，c12-CLA）对共轭亚油酸异构体的抑制作用，以防止前胃肿瘤的形成和化学预防机制。方法：建立由B（a）P诱导的昆明小鼠前胃肿瘤模型。计算前胃中的肿瘤数目和每个肿瘤的直径；用TBARS法测定小鼠血浆丙二醛（MDA）。 TUNEL法检测前胃肉瘤细胞凋亡，Western Blotting法检测前胃肉瘤中MEK-1，ERK-1，MKP-1蛋白的表达。结果：B（a）P组，纯度为c9，t11-CLA组，纯度为c9，t11-CLA组，纯度为98％，t10，C12-CLA组的肿瘤发生率分别为100％，75.0％P > 0.05），分别为69.2％（P <0.05）和53.8％（P <0.05），并且两种CLA异构体的纯度为98％对前胃癌的影响显着; CLA对荷瘤小鼠的平均肿瘤数无影响，但显着降低了肿瘤的大小，纯度为75％的c9，t11-CLA组，98％纯度的c9，t11-CLA组和98％的小鼠的肿瘤平均直径纯度t10％，B（a）P组c12-CLA组为0.157 + -0.047 cm，0.127 + -0.038 cm和0.128 + -0.077cm（P <0.05）和0.216 + -0.088 cm;在纯度为75％的c9，t11-CLA组，纯度为98％的c9，t11-CLA组和75％纯度的c9中，CLA还可以显着增加144.00 + -20.31、153.75 + -23.25、157.25 + -15.95（P <0.05）的凋亡细胞数。纯度t10，c12-CLA组为98％（BP组为30.88 + -3.72）;但是纯度为75％的c9，t11-CLA和两种异构体（纯度为98％）对肿瘤大小和凋亡细胞数量的影响没有显着差异；血浆中的MDA水平分别提高了75％纯度c9，t11-CLA，98％纯度c9，t11-CLA和98％纯度t10，c12-CLA。纯度75％的c9，t11-CLA表现出较强的抑制作用； CLA还可以抑制ERK-1蛋白的表达并促进MKP-1蛋白的表达，但未观察到CLA对MEK-1蛋白的影响。结论：纯度为98％的两种异构体对癌发生的抑制作用较强。然而，CLA对癌变的抑制机制是复杂的，这可能是由于小鼠血浆MDA增加，诱导了肿瘤组织中的细胞凋亡。 CLA对ERK-1和MKP-1表达的影响可能是抑制CLA对肿瘤的作用机制之一。

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