Effects of Selenium-Enriched Probiotics on Lipid Metabolism, Antioxidative Status, Histopathological Lesions, and Related Gene Expression in Mice Fed a High-Fat Diet
Effects of Selenium-Enriched Probiotics on Lipid Metabolism, Antioxidative Status, Histopathological Lesions, and Related Gene Expression in Mice Fed a High-Fat Diet
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富硒益生菌对高脂饮食小鼠的脂质代谢、抗氧化状态、组织病理学病变和相关基因表达的影响。
DOI：
10.1007/s12011-015-0552-8
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发表时间：
2016-06-01
影响因子：
3.9
通讯作者：
Huang, Kehe
中科院分区：
文献类型：
--
作者：
Nido, Sonia Agostinho;Shituleni, Shituleni Andreas;Huang, Kehe
将80只雌性白化病小鼠随机分为5组（n = 16）：（A）正常对照组;（B）高脂饮食组;（C）高脂饮食+益生菌组;（D）高脂饮食+亚硒酸钠组;（E）高脂饮食+富硒益生菌组。A、B、C、D、E组日粮硒含量分别为0.05、0.05、0.05、0.3、0.3 μ g/g。C组和E组中所含益生菌的量相似（嗜酸乳杆菌0.25 x 10（11）/mL和酿酒酵母0.25 x 10（9）/mL菌落形成单位（CFU））。高脂日粮由15%猪油、1%胆固醇、0.3%胆酸和83.7%基础日粮组成。实验结束后，采集血液和肝脏样品，测定脂质代谢、抗氧化状态、组织病理学改变和相关基因表达。结果表明，与对照组相比，HFD显著增加了小鼠的体重和肝脏损伤，而P、SS或SP补充减轻了小鼠的体重和肝脏损伤。添加P、SS或SP还显著逆转了HFD引起的丙氨酸氨基转移酶（AST）、天冬氨酸氨基转移酶（ALT）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL）、总蛋白（TP）、高密度脂蛋白（HDL）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和丙二醛（MDA）水平的变化。通常，添加P、SS或SP上调肉毒碱棕榈酰转移酶-I（CPT 1）、肉毒碱棕榈酰转移酶II（CPT 2）、乙酰辅酶A乙酰转移酶II（ACAT 2）、酰基辅酶A氧化酶（ACOX 2）和过氧化物酶体增殖物激活受体α（PPR α）的mRNA表达。（过氧化物酶体增殖物激活受体α）和下调的mRNA表达的脂肪酸合成酶（FAS），脂蛋白脂酶（LPL），过氧化物酶体增殖物激活受体γ（PPAR γ）和参与脂质代谢的固醇调节元件结合蛋白-1（SREBP 1）。其中，添加SP在改善喂食HFD的小鼠的脂质代谢、抗氧化状态、组织病理学病变和相关基因表达方面具有最大效果。
A total of 80 female albino mice were randomly allotted into five groups (n = 16) as follows: (A) normal control, (B) high-fat diet (HFD),; (C) HFD + probiotics (P), (D) HFD + sodium selenite (SS), and (E) HFD + selenium-enriched probiotics (SP). The selenium content of diets in groups A, B, C, D, and E was 0.05, 0.05, 0.05, 0.3, and 0.3 mu g/g, respectively. The amount of probiotics contained in groups C and E was similar (Lactobacillus acidophilus 0.25 x 10(11)/mL and Saccharomyces cerevisiae 0.25 x 10(9)/mL colony-forming units (CFU)). The high-fat diet was composed of 15 % lard, 1 % cholesterol, 0.3 % cholic acid, and 83.7 % basal diet. At the end of the 4-week experiment, blood and liver samples were collected for the measurements of lipid metabolism, antioxidative status, histopathological lesions, and related gene expressions. The result shows that HFD significantly increased the body weights and liver damages compared to control, while P, SS, or SP supplementation attenuated the body weights and liver damages in mice. P, SS, or SP supplementation also significantly reversed the changes of alanine aminotransferase (AST), aspartate aminotransferase (ALT), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), total protein (TP), high-density lipoprotein (HDL), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalasa (CAT), and malondialdehyde (MDA) levels induced by HFD. Generally, adding P, SS, or SP up-regulated mRNA expression of carnitine palmitoyltransferase-I (CPT1), carnitine palmitoyltransferase II (CPT2), acetyl-CoA acetyltransferase II (ACAT2), acyl-coenzyme A oxidase (ACOX2), and peroxisome proliferator-activated receptor alpha (PPAR alpha) and down-regulated mRNA expression of fatty acid synthase (FAS), lipoprotein lipase (LPL), peroxisome proliferator-activated receptor gamma (PPAR gamma), and sterol regulatory element-binding protein-1 (SREBP1) involved in lipid metabolism. Among the group, adding SP has a maximum effect in improving lipid metabolism, antioxidative status, histopathological lesions, and related gene expression in mice fed a HFD.