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1.
目的观察膳食n6n3脂肪酸比值对淋巴细胞脂肪酸构成及细胞功能的影响。方法BALBc小鼠随机分为5组n6n3比值分别为1(A组)、75(B组)、15(C组)、30(D组)和正常对照组,其中实验组S∶M∶P模拟中国居民膳食脂肪酸摄入的S∶M∶P为1∶15∶1,正常对照组为AIN93G配方的1∶15∶37。基础饲料采用AIN93G配方,脂肪酸构成以食用油脂调配。饲养12周。测定小鼠T淋巴细胞功能,脾淋巴细胞脂肪酸构成、PGE2水平。结果n6n3比值接近1时,小鼠T淋巴细胞增殖活性、CD4+、CD8+T细胞比例、培养上清IL2、PGE2水平显著降低;淋巴细胞C18∶2、C20∶4、n6PUFA含量显著减少;C22∶6、C16∶1、C18∶1、总MUFA含量明显高于其他实验组。淋巴细胞C22∶6含量与淋巴细胞增殖活性显著负相关;C20∶5含量与CD4+T淋巴细胞比例、IL2水平显著负相关;C16∶1含量与CD4+、CD8+T淋巴细胞比例显著负相关。结论小鼠脾淋巴细胞的脂肪酸构成受膳食脂肪酸构成的影响;n6n3比值为1组与比值为30的膳食组相比较,小鼠T淋巴细胞增殖活性受到抑制。  相似文献   

2.
不同脂肪酸构成比对小鼠血脂影响的实验研究   总被引:4,自引:0,他引:4  
目的:以小鼠饲料正常脂肪摄入量7.84%为基础,比较不同脂肪酸构成比对小鼠血脂水平的影响。方法:以小鼠正常饲料脂肪及脂肪酸构成为对照,分别设S/M/P比值为1∶1.7∶1.2和1∶1∶1的饲料,其中n-6/n-3比值在1~10∶1各设计4组,共10组, 喂小鼠10 w,测定血脂水平。结果: S/M/P为1∶1.7∶1.2, n-6/n-3在1~5∶1时TC和TC/HDL-C水平显著低于8∶1和10∶1组(P<0.05); S/M/P为1∶1∶1,n-6/n-3为1∶1时的TC和LDL-C水平显著低于其余各比值组(P<0.05);当n-6/n-3为10∶1时,S/M/P为1∶1.7∶1.2的TC、LDL-C、HDL-C以及TC/HDL-C和LDL-C/HDL-C水平均显著低于1∶1∶2组(P<0.05),S/M/P为1∶1∶2的LDL-C和TC/HDL-C水平显著低于1∶1∶1组(P<0.05)。结论: S/M/P现状1∶1.7∶1.2时,n-6/n-3在1~5∶1可维持血脂在较低水平;如脂肪酸构成比为1∶1∶1时,维持较低血脂所需的n-6/n-3为1∶1;在现状膳食n-6/n-3为10∶1时,S/M/P在1∶1.7∶1.2有利于维持低血脂。  相似文献   

3.
目的研究不同脂肪酸构成对小鼠血脂代谢、炎症和氧化应激及内皮细胞功能的影响。方法雄性KM小鼠随机分为5组,分别喂饲正常对照饲料、猪油高脂饲料和n-6/n-3多不饱和脂肪酸(PUFA)比值为1∶1、5∶1、20∶1的高脂饲料5周,比较各组小鼠血清中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、白介素-6(IL-6)、丙二醛(MDA)、超敏C反应蛋白(hsCRP)、肿瘤坏死因子(TNF-α)、脂质过氧化物(LPO)、8-异前列腺素F2α(8-isoPGF2α)、氧化型低密度脂蛋白(ox-LDL)、游离脂肪酸(FFA)、选择素(ES)和血管性血友病因子(v WF)的含量变化。结果猪油组LDL-C和非高密度脂蛋白胆固醇(non-HDL-C)水平显著高于其他各组(P0.05)。n-6/n-3 PUFA 1∶1组和5∶1组血清TG、TC水平显著低于猪油组(P0.05)。20∶1组血清FFA水平显著高于1∶1组和5∶1组(P0.05)。1∶1组和5∶1组血清炎症因子和氧化应激指标及ES水平均显著低于猪油组和20∶1组(P0.05)。5∶1组血清v WF水平显著低于猪油组和20∶1组(P0.05)。结论与猪油和高n-6/n-3 PUFA比值高脂饲料相比较,低n-6/n-3PUFA比值高脂饲料可改善小鼠脂代谢、炎症与氧化应激和内皮细胞功能。  相似文献   

4.
目的:探讨富含n-3多不饱和脂肪酸(PUFA)的肠外营养(PN)对脓毒症大鼠外周血T淋巴细胞亚群和血清炎性因子的影响。方法:将36只大鼠随机分为四组,颈静脉置管术2 d后行盲肠结扎穿孔术或假手术,1对照组:给予自由饮食;2NS组:给予等渗盐水输注+自由饮食;3SO组:给予富含豆油的标准肠外营养(PN)液;4FO组:给予富含PUFA的PN液。脓毒症5 d后,检测IL-6、IL-10和T细胞亚群等。结果:脓毒症5 d后,FO组大鼠外周血CD3+、CD4+、CD4+/CD8+与NS组和SO组比有所升高,但较对照组大鼠下降;与NS组大鼠比,FO组血清IL-6、IL-10、外周血Tregs比例有所下降。结论:应用富含n-3 PUFA的PN可降低脓毒症大鼠血清炎性因子和调控外周血T淋巴细胞亚群。  相似文献   

5.
目的探讨长期摄入高脂不同n-3/n-6多不饱和脂肪酸(PUFAs)构成比的饮食后,大鼠胰岛素敏感性及血清炎症因子表达水平的变化。方法 40只刚断乳雄性SD大鼠适应性喂养7天后,根据体重随机分为4组:空白对照组(基础饲料)、高脂组(猪油)、高脂1∶1组(n-3/n-6为1∶1)和高脂1∶4组(n-3/n-6为1∶4),每组10只。每周记录一次大鼠体重,喂养16周处死动物,检测大鼠血脂、血清胰岛素敏感性和血清炎症因子(IL-6、TNF-α和hs-CRP)表达水平。结果与空白对照组相比,其他3个组体重显著上升(P<0.05);高脂1∶1组胰岛素敏感性与空白对照组比较,差异无显著性,且显著高于高脂组和高脂1∶4组(P<0.05);与高脂组相比,高脂1∶1组血清TNF-α和hs-CRP表达水平显著下降(P<0.05)。结论长期摄取高多不饱和脂肪酸同样具有肥胖风险,提高n-3PUFAs在膳食构成中的比重可以有效抑制炎症因子表达,改善胰岛素敏感性,预防胰岛素抵抗的发生。  相似文献   

6.
目的 系统评价n-3多不饱和脂肪酸(n-3PUFAs)、n-6多不饱和脂肪酸(n-6PUFAs)及其比例与乳腺癌发病风险的关系。方法 系统检索Pubmed、Embase、Web of Science、知网、万方等数据库截止至2022年1月1日有关n-3及n-6多不饱和脂肪酸与乳腺癌关系的研究,对最终纳入的文献进行数据提取与质量评价,采用Stata 15.1软件进行Meta分析。结果 共纳入33项针对n-3及n-6PUFAs和乳腺癌发病风险关联的观察性流行病学研究,其中队列研究14项,病例对照研究20项,共纳入研究对象1 077 178例,患者19 207例。Meta分析结果显示:n-3多不饱和脂肪酸(OR=0.933,95%CI:0.858~1.014)、n-6多不饱和脂肪酸(OR=1.018,95%CI:0.914~1.133)与乳腺癌发病风险无统计学关联(P>0.05),而较高的n-6/n-3PUFAs比值会显著增加乳腺癌的发病风险(OR=1.166,95%CI:1.047~1.299,P=0.005)。结论 n-6/n-3多不饱和脂肪酸的比值与乳腺癌的发病风险呈正相关,提示合理的膳食脂肪摄入比可能会降低乳腺癌的患病风险。而n-3及n-6多不饱和脂肪酸与乳腺癌发病风险的单独效应关系尚不明确,仍需更多前瞻性实验流行病学证据进行支持。  相似文献   

7.
目的 探讨n-3多不饱和脂肪酸(n-3 polyunsaturated fatty acids,n-3 PUFAs)对饮食诱导肥胖小鼠肠道菌群的影响。方法 将30只3~4 周龄C57BL/ 6J雄性小鼠,随机分为3组(10只/组),分别给予高脂饲料、鱼油n-3 PUFAs高脂饲料(脂肪含量均为34.9%,供能比均为60%)以及正常脂饲料(脂肪来源于猪油和葵花籽油,脂肪含量为4.3%,供能比为10%)喂养16周。然后采集粪便,采用16sDNA-实时荧光定量PCR方法检测肠道菌群变化;取结肠组织,采用实时荧光定量PCR方法检测白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)以及单核细胞趋化蛋白-1(monocyte chemoattractant protein-1,MCP-1)的mRNA表达水平。结果 与正常脂饲料喂养对照组小鼠相比,高脂饲料诱导肥胖小鼠粪便中厚壁菌门及乳杆菌属的数量显著增多,而拟杆菌门、放线菌门、变形菌门以及双歧杆菌属的数量则显著减少(P<0.05)。两组肥胖小鼠相比,鱼油n-3 PUFAs高脂组肥胖小鼠的粪便双歧杆菌属数量明显增加,而乳杆菌属数量显著减少(P<0.05)。对结肠炎性因子mRNA表达水平检测显示,高脂饲料组肥胖小鼠的IL-1β、IL-6、TNF-α及MCP-1表达量较正常脂饲料组小鼠均明显升高(P<0.05),而IL-10的表达量无变化;鱼油n-3 PUFAs高脂饲料组肥胖小鼠的IL-1β、TNF-α较高脂饲料组肥胖小鼠有显著性的降低(P<0.05)。结论 鱼油n-3 PUFAs可以改善肥胖状态下的肠道菌群紊乱及肠道炎症状态。  相似文献   

8.
目的探讨高脂饲料喂养条件下,不同n-6/n-3多不饱和脂肪酸(polyunsaturated fatty acid,PUFA)构成比对大鼠脂联素和糖脂代谢及抗氧化能力的影响。方法50只雄性Wistar大鼠按体重随机分为5组:1个普通饲料组(脂肪供能比17%,n-6/n-3PUFA=5∶1)和4个高脂饲料组(脂肪供能比均为42%,n-6/n-3 PUFA构成比分别为1∶1、5∶1、10∶1、20∶1)。喂养12周后检测大鼠血糖和血脂(0、4、8和12周)、血清抗氧化指标(0和12周)以及睾周脂肪组织脂联素mRNA、蛋白表达和血清脂联素水平(12周)。结果大鼠各指标初始值组间差异均无统计学意义(P>0.05)。12周时,n-6/n-3PUFA 10∶1、20∶1组血糖显著高于对照组(P<0.05),4个高脂组血清总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)显著高于对照组(P<0.01),其中20∶1组TG显著高于其余3组(P<0.01);4个高脂组谷胱甘肽过氧化物酶和超氧化物歧化酶含量显著低于对照组(P<0.05),其中20∶1组下降最明显,丙二醛含量显著高于对照组(P<0.05),其中10∶1组上升最明显;20∶1组脂联素mRNA表达显著低于对照组、1∶1组和5∶1组(P<0.05),5∶1组脂联素蛋白表达水平显著高于其余高脂组(P<0.05),而20∶1组表达水平最低(P<0.05)。结论较低的n-6/n-3 PUFA构成比(1∶1和5∶1),有助于改善高脂饲料条件下大鼠糖脂代谢及抗氧化能力,提高脂联素表达。  相似文献   

9.
目的探讨孕及哺乳期摄入n-6/n-3多不饱和脂肪酸(PUFAs)变化对子代脑功能相关基因表达的影响。方法选用清洁级3~4周龄C57BL/6J雌性小鼠,随机分成5组,每组分别给予n-3 PUFAs缺乏和4种不同含量n-3 PUFAs(n-6/n-3 PUFAs比值分别为15∶1、5∶1、1∶1及1∶5)饲料喂养。小鼠12~14周龄时用常规饲料喂养的雄性小鼠与之合笼交配繁殖,仔鼠断乳后继续行母鼠相同饲料喂养,随访观察至生后7d、21d和12周龄时分批处死后取脑。然后在仔鼠生后21d断乳时,随机挑选7~9只n-3 PUFAs缺乏组的仔鼠用n-6/n-3 PUFAs(5∶1)组饲料喂养,至12周龄;同时随机挑选7~9只n-6/n-3 PUFAs(5∶1)组的仔鼠,改用n-3缺乏组饲料喂养,至12周龄;剩余仔鼠用与母鼠相同的饲料喂养,至12周龄;麻醉牺牲后,取脑置于-80℃条件下备用。采用实时荧光定量PCR技术测定脑皮质gfap、mbp、nse和nr2b基因mRNA的表达。结果在各年龄段小鼠中,饲料中添加n-3 PUFAs使各基因的表达量明显增加;不同比例的n-6/n-3PUFAs对基因表达的影响不同。孕期及哺乳期饲料缺乏n-3 PUFAs,即使断乳后的饲料中添加正常量的n-3 PUFAs,也不能使某些对脑功能起重要作用的基因的表达量升高至正常n-3 PUFAs喂养的小鼠。结果提示,孕期及哺乳期可能需要较高的n-3 PUFAs摄入(可能最优的n-6/n-3 PUFAs比例介于1∶5~1∶1之间),才能满足幼年期脑发育之需。结论孕及哺乳期n-3多不饱和脂肪酸(PUFAs)的适量摄入,有助于维持成年期脑功能相关基因的正常表达。  相似文献   

10.
n-6/n-3 PUFA对乳腺癌大鼠ER及p53表达影响   总被引:2,自引:2,他引:0  
目的 探讨不同比例的n-6/n-3多不饱和脂肪酸(PUFA)对N-甲基亚硝基脲(MNO)诱导的乳腺癌大鼠乳腺组织中雌激素受体(ER)和p53表达的影响.方法 雌性SD大鼠随机分为n-6 PuFA、10:1 n-6/n-3、5:1 n-6/n-3、1:1 n-6/n-3和正常对照5组,前4组以50mg/(kg·bw)MNU单次腹腔注射诱导乳腺肿瘤发生,正常对照组注射等体积无菌生理盐水.给药后立即分组喂养不同饲料,在8和18周时处死动物,RT-PCR和蛋白印迹(Western blot)技术检测各组大鼠乳腺组织ER和p53表达.结果 4组乳腺癌大鼠乳腺组织中ER和p53的表达均较正常对照组[(0.73±0.11),(0.08±0.01)]有所升高,其中n-6组最高((1.32±0.18),(1.43±0.56)],其余各组随n-6/n-3比值减小而下降,1:1 n-6/n-3组[(0.95±0.12),(0.12±0.06)]显著低于n-6组(P<0.05).结论 不同比例n-6/n-3多不饱和脂肪酸对MNU诱导的乳腺癌大鼠乳腺组织ER和p53的表达具有不同影响,1:1 n-6/n-3膳食脂肪酸构成能有效抑制乳腺癌大鼠乳腺组织ER和p53表达的升高.  相似文献   

11.
目的分析广州40~65岁居民膳食n-6/n-3脂肪酸比值与心血管疾病危险因素的关系。方法 40~65岁广州市民1133人,采用定量食物频数问卷调查对象的每日摄入食物种类和数量,计算能量和营养素摄入量,检测其红细胞膜脂肪酸构成、血脂及颈动脉内中膜厚度(IMT),分析n-6/n-3比值大小高Q3,中Q2,低Q1与血压、血脂和IMT的关系。结果 995人资料完整纳入分析。对象日均膳食总能量摄入为9.10±2.09MJ、脂肪供能比为(34.3±7.9)%。膳食n-6/n-3脂肪酸比值为(29.74±22.71):1,红细胞膜n-6/n-3脂肪酸比值为(2.7±1.0):1,膳食SFA:MUFA:PUFA为1:1.5:1。膳食n-3脂肪酸摄入量与红细胞膜n-3构成比、膳食n-6/n-3比值与红细胞膜n-6/n-3比值均呈显著正相关关系。膳食n-6/n-3比值最高组Q3(>31.16)对象的收缩压、TC和IMT水平显著高于最低组Q1(<17.40);红细胞膜n-6/n-3比值最高组Q3(>3.04)和中间组Q2(2.18~3.03)对象的收缩压、舒张压、TC、LDL-C及IMT水平均显著高于最低组Q1(≤2.17)。结论广州市40~65岁居民膳食n-6/n-3脂肪酸比值约为30:1;该比值小于17.40:1时,有较低的血压,总胆固醇及IMT水平。  相似文献   

12.
Summary Background Indian Asians living in Western Countries have an over 50 % increased risk of coronary heart disease (CHD) relative to their Caucasians counterparts. The atherogenic lipoprotein phenotype (ALP), which is more prevalent in this ethnic group, may in part explain the increased risk. A low dietary long chain n-3 fatty acid (LC n-3 PUFA) intake and a high dietary n-6 PUFA intake and n-6:n-3 PUFA ratio in Indian Asians have been proposed as contributors to the increased ALP incidence and CHD risk in this subgroup. Aim To examine the impact of dietary n-6:n-3 PUFA ratio on membrane fatty acid composition, blood lipid levels and markers of insulin sensitivity in Indian Asians living in the UK. Methods Twentynine males were assigned to either a moderate or high n-6:n-3 PUFA (9 or 16) diet for 6 weeks. Fasting blood samples were collected at baseline and 6 weeks for analysis of triglycerides, total-, LDL- and HDL-cholesterol, non-esterified fatty acids, glucose, insulin, markers of insulin sensitivity and C-reactive protein. Results Group mean saturated fatty acid, MUFA, n-6 PUFA and n-3 PUFA on the moderate and high n-6:n-3 PUFA diets were 26 g/d, 43 g/d, 15 g/d, 2 g/d and 25 g/d, 25 g/d, 28 g/d, 2 g/d respectively. A significantly lower total membrane n-3 PUFA and a trend towards lower EPA and DHA levels were observed following the high n-6:n-3 PUFA diet. However no significant effect of treatment on plasma lipids was evident. There was a trend towards a loss of insulin sensitivity on the high n-6:n- 3 PUFA diet, with the increase in fasting insulin (P = 0.04) and HOMA IR [(insulin x glucose)/ 22.5] (P = 0.02) reaching significance. Conclusion The results of the current study suggest that, within the context of a western diet, it is unlikely that dietary n-6:n-3 PUFA ratio has any major impact on the levels of LC n-3 PUFA in membrane phospholipids or have any major clinically relevant impact on insulin sensitivity and its associated dyslipidaemia. Source of support: This project was funded by the Food Standards Agency (FSA), UK.  相似文献   

13.
The effects of a 47-week diet of butter or safflower oil as fat in combination with casein or soy protein as protein were observed for the serum concentrations of lipids and fatty acid compositions in rat serum and heart. Serum total cholesterol (Chol) did not differ among the four experimental diet groups. In the butter groups, significantly higher low-density lipoprotein (LDL)-Chol and lower high-density lipoprotein (HDL)-Chol were observed than in the safflower oil groups (p<0.005, respectively). Higher levels of α-tocopherol were found in the butter groups than in the safflower oil groups (p<0.05) and in the casein groups than in the soy protein groups (p<0.01). In comparison with the safflower oil groups, the butter groups showed higher n-3 polyunsaturated fatty acids (PUFA) contents and lower n-6 PUFA contents in serum and the hearts (p<0.005). The ratios of n-3/n-6 PUFA in the butter groups in serum, 0.26 and 0.18, and in the hearts, 0.37 and 0.36, (butter-casein diet and butter-soy protein diet, respectively) were higher than those of the safflower oil groups of under 0.01 in serum and 0.02 and 0.03 in the hearts (safflower oil-casein diet and safflower oil-soy protein diet, respectively) (p<0.005). In the soy protein groups, higher n-3 PUFA contents in the hearts were found than those of the casein groups (p<0.05). This study suggested that the butter diet induces higher levels of n-3 PUFA and a higher n-3/n-6 PUFA ratio than the safflower oil diet in rat serum and hearts over a long feeding period.  相似文献   

14.
To survey risk factors in coronary heart disease, we compared serum fatty acid composition and lipids for university students in Japan (33 males and 29 females) and in the Netherlands (20 males and 19 females). No significant differences were found between the mean levels of cholesterol (Chol) and triglycerides (TG) between the subjects in the two countries. The mean levels of polyunsaturated fatty acid (PUFA), monounsaturated fatty acid (MUFA) and saturated fatty acid (SFA) of Japanese students were similar to those of the Dutch students. In both countries, the levels of Chol showed a positive correlation with the levels of PUFA, n-6 PUFA, linoleic acid (C18:2n-6), and arachidonic acid (AA, C20:4n-6) but no correlation with the percentages of PUFA and the ratio of PUFA/SFA. On the other hand, the TG levels correlated inversely with the percentage of PUFA and the ratios of PUFA/SFA in both countries. When compared to those of Japanese students, low eicosapentaenoic acid (EPA, C20:5n-3) and high AA were found in the Dutch students (p < 0.001, respectively). The total amounts of n-3 PUFA in the Dutch were significandy lower than those in the Japanese (p < 0.001) but no differences among those of n-6 PUFA. The ratios of EPA/AA and n-3/n-6 PUFA of the Dutch students were lower than those of the Japanese students (p < 0.001, respectively). The ratio of EPA/AA showed a positive correlation with EPA but not with AA in both countries. The levels of Toc which will decrease the risk of coronary vascular disease (CVD) were lower in Japan than those in the Dutch in both sexes (p < 0.01, respectively). These results suggest that the low EPA and high AA levels and the low n-3/n-6 PUFA ratio may lead to greater incidence of CVD.  相似文献   

15.
目的研究不同n-3/n-6配比脂肪酸对大鼠磷酸腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白及活性表达的影响。方法58只SD大鼠适应性喂养7d后,尾静脉取血。根据血清总胆固醇水平随机分为:空白(基础饲料);高脂(高脂饲料);高脂1:1(高脂饲料+n-3/n-6=1:1配方油);高脂1:5(高脂饲料+n3/n6=1:5配方油);低脂1:1(脱脂基础饲料+n-3/n-6=1:1配方油);低脂1:5(脱脂基础饲料+n3/n6=1:5配方油)6组,喂养45d,观察大鼠摄食与体重增长。于实验前1d,15d,30d,45d分别各取血测血清总胆固醇水平,于D45处死动物。Western blotting分别分析肝和下丘脑组织中AMPK-α总蛋白及其活性表达。结果添加PUFA的4个比例组血清TC、体重与高脂组相比,显著降低,且低脂2个比例组和高脂1:1组均与高脂1:5组相比有显著差异。添加PUFA的4个比例组均与高脂组相比,大鼠下丘脑AMPK-α总蛋白表达水平明显降低,肝AMPK-α蛋白表达水平均比高脂组明显升高。结论PUFA改善血脂可能是通过增加肝AMPK表达,抑制下丘脑AMPK表达,增加肝脂肪酸氧化和抑制食欲,影响血脂代谢。  相似文献   

16.
17.
Dietary n-3 polyunsaturated fatty acids (PUFA) reduce coronary heart disease (CHD) complications, such as chronic arrhythmia and sudden cardiac death. Improved myocardial resistance to ischemia-reperfusion injury results in smaller myocardial infarction, which is a major factor in the occurrence of CHD complications. We hypothesized that a specific dietary fatty acid profile (low in saturated and n-6 PUFA but high in plant and marine n-3 PUFA) may improve myocardial resistance to ischemia-reperfusion injury and reduce infarct size. To test this assumption, we used a well-defined rat model of myocardial infarction. Based on our results, in comparison to a diet that is high in either saturated or n-6 PUFA but poor in plant and marine n-3 PUFA, a diet that is low in saturated fats and n-6 PUFA but rich in plant and marine n-3 PUFA results in smaller myocardial infarct size (P < .01). The effects of the 3 diets were also examined by analyzing the fatty acid composition of plasma, erythrocyte cell membranes, and the phospholipids of myocardial mitochondria. The results show a great accumulation of n-3 PUFA and a parallel decrease in arachidonic acid, the main n-6 PUFA, in plasma, cell membranes, and cardiac mitochondria (P < .0001). We conclude that improved myocardial resistance to ischemia-reperfusion may be one of the critical factors explaining the protective effects of dietary n-3 PUFA against CHD complications in humans. In addition to increasing n-3 PUFA intake, an optimal dietary pattern aimed at reducing cardiovascular mortality should include a reduction of the intake of both saturated and n-6 PUFA.  相似文献   

18.
目的 探讨核受体基因表达在不同膳食脂肪酸影响大鼠乳腺癌发生中的作用。方法用8种不同膳食脂肪酸(饱和脂肪酸、单不饱和脂肪酸、n-6多不饱和脂肪酸、n-3多不饱和脂肪酸、1:1n-6/n-3多不饱和脂肪酸、5:1n-6/n-3多不饱和脂肪酸、10:1n-6/n-3多不饱和脂肪酸、1:2:1饱和脂肪酸/单不饱和脂肪酸/多不饱和脂肪酸其中n-6/n-3多不饱和脂肪酸1:1)喂养SD雌性幼年大鼠,采用50mg/kg的甲基亚硝基脲单次腹腔注射诱导大鼠乳腺癌发生,电镜观察大鼠乳腺细胞结构变化,BrdU体内标记法检测大鼠乳腺细胞增殖活性,RT—PCR分析乳腺组织过氧化物酶增殖活化受体(PPARβ和PPARγ)mRNA表达。结果 无乳腺癌诱发的各对照和n-3多不饱和脂肪酸诱癌组大鼠乳腺细胞超微结构正常,细胞增殖活性低。而有大鼠乳腺癌诱发的组织细胞内可见明显的腺癌标志,且高乳腺癌诱发的饱和脂肪酸、单不饱和脂肪酸、n-6多不饱和脂肪酸、5:1n-6/n-3多不饱和脂肪酸、10:1n-6/n-3多不饱和脂肪酸和1:2:1饱和脂肪酸/单不饱和脂肪酸/多不饱和脂肪酸喂养组大鼠乳腺细胞增殖活性升高(BrdU阳性率为21%~22%),但1:1n-6/n-3多不饱和脂肪酸低诱癌组乳腺细胞增殖活性明显降低上述高乳腺癌诱发组(BrdU阳性率为13%,P〈0.05)。此外,过氧化物酶增殖活化受体作为与脂代谢密切相关的细胞核受体基因,1:1n-6/n-3多不饱和脂肪酸低诱癌组较相应对照组上调PPARβ和PPARγ mRNA表达力度明显弱于高乳腺癌诱发组。结论 不同膳食脂肪酸对PPAR基因表达的调节截然不同,这可能是差异性调节大鼠乳腺癌发生的分子机制之一。  相似文献   

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