乳双歧杆菌XLTG11缓解环磷酰胺致小鼠免疫功能损伤

该研究探讨乳双歧杆菌XLTG11对免疫功能损伤模型小鼠免疫功能的影响。采用环磷酰胺（CTX）构建小鼠免疫损伤模型,设立空白组和模型组,灌服生理盐水,阳性对照组,灌服盐酸左旋咪唑（LEV）（10 mg/kg）,给药组灌服不同浓度乳双歧杆菌XLTG11（1×106、1×107、1×108、1×109 CFU）,连续28 d,测定各组小鼠免疫功能相关指标。各剂量组乳双歧杆菌XLTG11可以拮抗CTX对小鼠胸腺的损伤,胸腺指数分别比模型组提高37.37%、43.43%、56.56%和84.84%（p<0.05）;增加小鼠足跖肿胀程度,足跖厚度分别比模型组提高38.24%、50.00%、55.89%和94.12%（p<0.05）;提高小肠绒毛高度,增加杯状细胞数目（p<0.05）,其中1×109 CFU剂量组小肠绒毛高度提高20.82%（p<0.01）,杯状细胞数目提高51.23%（p<0.01）;升高血清免疫球蛋白和细胞因子水平（p<0.05）,以IgA、IL-2和TNF-α水平升高最为显著,1×109 CFU剂量组IgA水平升高20.03%（p<0.001）,IL-2水平升高35.94%（p<0.001）,TNF-α水平升高14.50%（p<0.05）。乳双歧杆菌XLTG11具有增强小鼠免疫功能作用,且呈剂量依赖性。该研究为益生菌保健食品开发和使用提供理论依据。     

Effects of Lactobacillus Casei YBJ02 on Lipid Metabolism in Hyperlipidemic Mice

Traditionally fermented yak yogurt as a Tibetan dairy product is high not only in nutrients but also in probiotics. A probiotic strain with a potential lipid reducing effect was isolated from yak yogurt. An animal model for hyperlipidemia was evaluated using the blood index and expression levels of lipid metabolism‐related proteins in mice to determine the effect of Lactobacillus casei YBJ02 (LC‐YBJ02) on lipid metabolism in hyperlipidemic mice and the underlying mechanism. LC‐YBJ02 at different concentrations exhibited certain inhibitory effects on the increase in blood lipid in mice. Particularly, high concentrations of LC‐YBJ02 can reduce the cholesterol, triglycerides, and low‐density lipoprotein content; however, no significant effect on the high‐density lipoprotein of the body has been reported. LC‐YBJ02 can effectively increase the reduction in cholesterol level by fecal excretion. In this study, the gene‐affecting mouse obesity was determined using experimental results in mice. The expression levels of peroxisome proliferator‐activated receptor γ (PPARγ), CCAAT enhancer binding protein alpha (CEBP)/α, sterol regulatory element binding protein (SREBP)‐1c, and FAS could improve because of the high‐fat diet in kidney fat. Bacteria at different concentrations could also decrease these expression levels. Specifically, the high concentration of LC‐YBJ02 could suppress the expression of PPARγ, CEBP/α, and SREBP‐1c; however, the expression of FAS was not significantly inhibited. PPARγ and FAS expression levels in the liver were low, but no significant difference was indicated. CEBP/α and SREBP‐1c expression in mouse liver was further detected by Western blot analysis; CEBP/α was considerably low and could not be detected. On the basis of these results, LC‐YBJ02 could be used as probiotics through its lipid reduction effects.     

乳双歧杆菌V9对头孢曲松钠作用小鼠肠道菌群的变化

该研究主要探讨了乳双歧杆菌V9对头孢曲松钠作用的小鼠肠道菌群的变化。头孢曲松钠连续灌胃5 d建立小鼠肠道菌群失调的模型,然后随机分为4组,分别为模型组及低、中和高剂量组。低、中和高剂量组灌胃不同剂量乳双歧杆菌V9溶液,另设正常对照组,与模型组灌胃等体积生理盐水,连续灌胃23 d。灌胃结束后,采集小鼠的粪便进行活菌计数和16S rDNA测序,检测粪便中微生物组成及分布,测定血清中IL-1β、IL-6、TNF-α以及IL-2的含量,测定小肠及肝脏组织中SOD、MDA、GSH、GSH-Px的含量,HE染色观察小鼠小肠组织病理学变化。结果表明,灌胃乳双歧杆菌V9溶液后,中、高剂量组IL-1β、IL-6、TNF-α及IL-2的含量分别显著降低31.73、17.04、12.57及31.71 pg/mL;高剂量组小肠及肝脏组织中MDA含量显著降低（p<0.01）,中、高剂量组SOD、GSH及GSH-Px均极显著升高（p<0.01）。同时,乳双歧杆菌V9使得头孢曲松钠导致的小鼠肠道菌群失调得到明显改善,粪便活菌计数显示高剂量组肠杆菌数量显著降低0.34 lg cfu/g,乳杆菌及双歧杆菌数量显著增加,分别增加0.40 lg cfu/g和0.26 lg cfu/g。拟普雷沃菌属和魏斯氏菌丰度显著降低（p<0.01）。说明乳双歧杆菌V9对由头孢曲松钠引起的肠道菌群失衡具有一定的调节作用,并调节菌群多样性。     

蛋氨酸限制和胶原蛋白肽对高脂饮食小鼠脂代谢和氧化应激的联合作用

目的：研究饮食蛋氨酸限制（methionine restriction,MR）和胶原蛋白肽对高脂饮食小鼠肝脏脂代谢和氧 化应激的联合作用。方法：将36 只C57BL/6雄性小鼠随机分为4 组：低脂正常饮食组（ND组）、高脂饮食组（HF 组）、高脂蛋氨酸限制组（MR组）及高脂蛋氨酸限制和胶原蛋白肽联合作用组（PMR组）。每周监测体质量,22 周实验结束,测定血浆中的甘油三酯（triglyceride,TG）、总胆固醇（total cholesterol,TC）、高密度脂蛋白胆固 醇、低密度脂蛋白胆固醇和游离脂肪酸（free fatty acid,FFA）含量;测定肝脏中的TG和TC含量;测定肝脏和血浆 中的总抗氧化能力（total antioxidant capacity,T-AOC）、谷胱甘肽过氧化物酶（glutathion peroxidase,GSH-Px） 活力和丙二醛（malondialdehyde,MDA）含量;实时荧光定量聚合酶链式反应（quantitative real time polymerase chain reaction,qPCR）测定脂代谢相关基因固醇调节元件结合蛋白1c（sterol regulatory element-binding protein 1c,SREBP1c）、脂肪酸合成酶（fatty acid synthase,FAS）、乙酰辅酶A羧化酶（acetyl CoA-carboxylase 1, ACC-1）、胆固醇7α-羟化酶（cholesterol 7α-hydroxylase,CYP7A1）、对肉碱酰基转移酶1（carnitine palmityl transferase 1,CPT1）和过氧化物酶体增殖物激活受体α（peroxisome proliferator activated receptor α,PPARα）的表 达。结果：与HF组相比,MR组小鼠体质量、肝脏中的TG和TC含量极显著降低（P＜0.01）;肝脏脂肪合成相关基 因FAS和SREBP1c极显著下调（P＜0.01）,ACC-1显著下调（P＜0.05）;脂肪分解相关基因CYP7A1和PPARα极显 著上调（P＜0.01）,CPT1显著上调（P＜0.05）;肝脏中T-AOC和GSH-Px活力显著增加（P＜0.05）,MDA和活 性氧含量极显著降低（P＜0.01）;血浆中T-AOC和GSH-Px活力极显著增加（P＜0.01）,血浆MDA和全血活性氧 含量极显著降低（P＜0.01）。与MR组相比,PMR组体质量和肝脏中的TG含量极显著降低（P＜0.01）;血浆中的 TG和TC含量显著降低（P＜0.05）;脂肪合成相关基因SREBP1c和ACC-1显著下调（P＜0.05）;脂肪分解相关基因 CPT1和PPARα显著上调（P＜0.05）;肝脏GSH-Px活力显著增加（P＜0.05）。结论：蛋氨酸限制饮食能显著降低 高脂饮食小鼠血脂和肝脏脂肪积累,增强肝脏抗氧化能力,且蛋氨酸限制与胶原蛋白肽的联合作用更能显著降低高 脂饮食小鼠血脂和肝脏脂肪积累,增强肝脏抗氧化能力。     

咖啡碱和绿原酸对高脂饮食小鼠体质量、脂类沉积及肝脏脂质代谢基因表达的影响

研究咖啡主要成分咖啡碱和绿原酸对高脂饮食诱导的肥胖小鼠体质量、脂类沉积及肝脏脂类代谢基因表达的影响。50只雌性ICR小鼠被随机分成5组:对照组、高脂组、咖啡碱、绿原酸、咖啡碱+绿原酸,给药组分别在饮水中添加0.05%咖啡碱、0.2%绿原酸、0.05%咖啡碱+0.2%绿原酸,饲养14周。饲养期间每周测1次体质量。饲养结束后心脏采血,摘取脏器和腹腔内脂肪(intraperitoneal adipose tissues,IPAT)并称质量。测定血糖浓度、血中及肝脏中脂质含量。通过实时定量聚合酶链式反应测定肝脏中脂质代谢相关基因AMPK、HMG-CoAr、FASN、ACO的mRNA表达量。与高脂组相比,咖啡碱+绿原酸能明显抑制小鼠体质量和IPAT质量的增加;咖啡碱、咖啡碱+绿原酸明显降低血糖和总胆固醇浓度;绿原酸投喂小鼠血中低密度脂蛋白胆固醇浓度显著降低,而血中游离脂肪酸浓度上升;咖啡碱、咖啡碱+绿原酸显著降低肝脏中总胆固醇和甘油三酯的含量;咖啡碱和咖啡碱+绿原酸使AMPK基因相对表达量显著上升,FASN基因相对表达量显著下降;3组给药组的ACO基因相对表达量显著上升,HMG-CoAr基因相对表达量显著下降。咖啡碱+绿原酸的减肥作用可能通过调节肝脏脂质代谢相关基因的表达,来降低血中和肝脏中脂类的含量,抑制脂肪沉积,抑制小鼠体质量增加,且它们有协同作用。     

实时荧光定量PCR法鉴定婴幼儿配方乳粉中动物双歧杆菌乳亚种

该研究通过系统发育树分析确定目标基因,并设计引物和探针,建立一种婴幼儿配方乳粉中动物双歧杆菌乳亚种（Bifidobacterium animalis subsp. lactis）的实时荧光定量聚合酶链式反应（RT-fqPCR）鉴定方法。通过特异性、灵敏性和抗干扰实验对该方法进行验证,并对市售的64份标识含有动物双歧杆菌乳亚种的婴幼儿配方乳粉样品进行检测。结果表明,atpD基因在动物双歧杆菌乳亚种间具有较高的种间特异性,种间差异率＞10%,确定其为目标基因。基于该基因建立的RT-fqPCR方法能够特异性的检测动物双歧杆菌乳亚种,检测绝对灵敏度可以达到1 pg/μL,相对灵敏度可以达到103 CFU/mL;基因水平和培养物水平抗干扰能力良好。采用该方法从64份标识含有动物双歧杆菌乳亚种的乳粉样品中均能检测出动物双歧杆菌乳亚种,表明基于atpD基因建立的RT-fqPCR方法能够快速准确的对动物双歧杆菌乳亚种进行检测。     

Lactobacillus delbrueckii subsp. bulgaricus和Streptococcus thermophilus接种比例对Bifidobacterium lactis益生菌发酵乳品质的影响

将Lactobacillus delbrueckii subsp.bulgaricus ND02(LB-ND02)和Streptococcus thermophilus ND03(ST-ND03)按1∶1、1∶10、1∶100、1∶1000接种于脱脂乳中,同时接入益生菌Bifidobacterium lactis V9(B.lactis V9,接种量为2.0×107g-1),于42℃进行发酵。通过对发酵及贮藏过程中发酵乳指标的测定,评价LB-ND02和ST-ND03的接种比例对发酵乳品质的影响。结果表明,随着LB-ND02接种比例减小,凝乳时间显著延长,B.lactis V9活菌数显著提高。4℃贮藏28 d后,随LB-ND02接种比例减小,B.lactis V9存活率差异显著,后酸化也显著减弱。研究发现,LB-ND02和ST-ND03的接种比例,显著影响发酵乳的发酵时间、B.lactis V9活菌数、后酸化及黏度。     

Phenolic Bioactive Modulation by Lactobacillus acidophilus Mediated Fermentation of Cherry Extracts for Anti-Diabetic Functionality,Helicobacter pylori inhibition and Probiotic Bifidobacterium longum Stimulation

Cherry juice from one cultivar was fermented for 0, 24, 48, and 72 h using Lactobacillus acidophilus, and its effects related to management of hyperglycemia, hypertension, inhibition of Helicobacter pylori, and proliferation of probiotic Bifidobacterium longum were evaluated using in vitro models. Cherry extract was fermented by initially adjusting the pH to 6.0 and at the natural acidic pH. Analysis was carried out by adjusting the pH and at fermented acidic pH at each time point from each of the two samples. Total soluble phenolics decreased over a period of 72 h for initial pH adjusted samples whereas it increased or remained constant for natural acidic pH samples. DPPH linked antioxidant activity and α-glucosidase inhibitory activity decreased for samples where final pH was adjusted whereas it increased for natural acidic pH samples. Fermentation led to a decrease in hypertension-relevant ACE inhibitory activity for all samples. Natural acidic pH samples had Helicobacter pylori inhibitory activity at 24, 48 and 72 h. Based on the rationale that simple phenolics in cherry could behave as proline analogs, the potential recovery of the pathogen from inhibition was evaluated with of addition of 0.5 mM proline in the medium. A proline induced growth recovery was observed indicating that the mechanism of inhibition is related to proline dehydrogenase based oxidative phosphorylation. Overall, no inhibition was observed when samples that had H. pylori inhibitory activity were further evaluated for their effect on probiotic Bifidobacterium longum.     

发酵陈皮黑茶改善高脂饮食诱导的小鼠糖脂代谢紊乱

本研究通过高脂饮食诱导C57BL/6J小鼠建立代谢紊乱模型,探究发酵陈皮黑茶对小鼠的体质量增长、空腹血糖水平、糖耐量、胰岛素水平、血脂水平以及肠道菌群变化等的影响.结果表明,与模型对照组相比,0.75～3.00 g/kg mb的发酵陈皮黑茶干预可以有效降低高脂饮食诱导的小鼠空腹血糖水平,3.00 g/kg mb的发酵陈...     

乳酸链球菌L16对感染金黄色葡萄球菌小鼠肠道菌群的调节作用

为研究乳酸链球菌L16对金黄色葡萄球菌感染小鼠肠道菌群结构的恢复情况,采用高通量测序技术,构建小鼠肠道微生物的16S rRNA基因测序文库,通过菌群结构图、等级丰度分布曲线、热图、稀释性曲线图、维恩图等,分析预防组、治疗组、正常组和模型组小鼠的肠道菌群组成和生物多样性。结果:模型组中脱铁杆菌门(12.67%)显著升高,菌群结构异常。预防组中厚壁菌门(49.03%)和拟杆菌门(43.15%)的相对丰度接近正常组(44.75%;42.08%)。结论:乳酸链球菌L16能预防金黄色葡萄球菌感染小鼠肠道,调节肠道菌群结构。     

不同色型藜麦对高脂膳食小鼠脂代谢的影响及机制

为了探索同一产地、不同色型藜麦对高脂膳食小鼠脂代谢的影响。将50 只SPF级雄性健康小鼠适应性喂养7 d后,根据体质量随机分为空白对照组、模型组、白藜麦组、黑藜麦组和红藜麦组,干预时间为8 周。实验结束后,测定其Lee’s指数、腰围、腹部脂肪质量,血清和肝脏组织的总胆固醇（total cholesterol,TC）、甘油三酯（triglyceride,TG）、低密度脂蛋白胆固醇（low-density lipoprotein cholesterol,LDL-C）、高密度脂蛋白胆固醇（low-density lipoprotein cholesterol,HDL-C）等脂代谢相关生理生化指标;并采用实时荧光定量聚合酶链式反应（quantitative real-time polymerase chain reaction,qPCR）和蛋白质免疫印迹检测肝脏胆固醇和脂质代谢关键基因mRNA和蛋白相对表达量。结果表明：与模型组相比,白、黑、红藜麦可降低小鼠Lee’s指数、腰围、腹部脂肪质量;显著下调小鼠血清、肝脏组织的TC和TG水平（P＜0.05）,显著上调小鼠肝脏组织的HDL-C水平（P＜0.05）;显著下调小鼠肝脏3-羟基-3甲基戊二酸单酰辅酶A还原酶（3-hydroxy-3-methylglutaryl CoA reductase,HMG-CoAr）和固醇调节元件结合蛋白（sterol regulatory element binding protein,SREBP）-1c的mRNA及蛋白相对表达量（P＜0.05）,其中白、黑、红藜麦的HMG-CoAr mRNA相对表达量分别下调了56.22%、72.55%和27.77%,蛋白相对表达量分别下降了53.02%、29.72%、29.80%;SREBP-1c mRNA相对表达量分别下调了62.96%、45.50%和21.27%,蛋白相对表达量分别下降了20.79%、23.97%、20.26%;明显提高AMP活化蛋白激酶α（AMP-activated protein kinase alpha,AMPKα）、低密度脂蛋白受体（low density lipoprotein receptor,LDL-R）、肝X受体（liver X receptor,LXR）、过氧化物酶体增殖物激活受体α（peroxisome proliferators-activated receptor-α,PPARα）和胆固醇7α-羟化酶（cytochrome P450 family 7 subfamily A member 1,CYP7A1）的mRNA相对表达量和LDL-R、PPARα的蛋白相对表达量,其中白、黑、红藜麦的LDL-R mRNA相对表达量分别升高了243.86%、273.04%和121.93%,蛋白相对表达量分别上调了18.02%、17.16%、22.45%;PPARα mRNA相对表达量分别升高了62.45%、87.54%和126.91%,蛋白相对表达量分别上调了54.26%、51.10%、33.82%。结论：不同色型藜麦均可改善高脂膳食小鼠脂代谢紊乱,其中白藜麦和黑藜麦效果优于红藜麦,其机制可能与降低胆固醇合成和减少脂肪酸从头合成有关。     

鱼胶原蛋白肽对高脂膳食小鼠肝脏脂肪代谢和氧化还原状态的影响

目的：研究鱼胶原蛋白肽（fish collagen peptides,FCPs）对高脂膳食（high-fat diet,HFD）小鼠肝脏脂肪代谢和氧化还原状态的影响。方法：54?只C57BL/6雄性小鼠按体质量随机分为正常膳食组（CON）、HFD组（HF）和FCPs干预HFD组（PHF）。每周记录各组小鼠体质量,并按体质量把每组小鼠随机均分为两批,分别在第11和22周宰杀,测定采食量、脂肪表观消化率;肝脏中甘油三酯（triglyceride,TG）、总胆固醇和游离脂肪酸（free fatty acid,FFA）含量;肝脏脂代谢相关基因乙酰辅酶A羧化酶1、脂肪酸合成酶、固醇调节元件结合蛋白1c、胆固醇7α-羟化酶（cholesterol 7α-hydroxylase 1,CYP7A1）、过氧化物激活受体α（peroxisome proliferator activated receptor α,PPARα）和肉毒碱棕榈酰基转移酶1（carnitine palmity1 transferase 1,CPT1）的mRNA表达水平,肝脏氧化还原状态相关指标活性氧自由基（reactive oxygen species,ROS）、丙二醛、总抗氧化能力（total antioxidant capacity,T-AOC）、谷胱甘肽过氧化物酶（glutathion peroxidase,GSH-Px）活力和还原型/氧化型谷胱甘肽的水平。结果：第22周时,与HF组相比,PHF组小鼠的采食量、脂肪和能量摄入显著增加（P＜0.05）,肝脏的TG、FFA、脂肪空泡和脂肪浸润面积比明显降低（P＜0.05）,脂肪分解关键基因CYP7A1、PPARα和CPT1的mRNA表达水平显著上调（P＜0.05）,肝脏的ROS水平显著降低（P＜0.05）,T-AOC水平和GSH-Px活力显著升高（P＜0.05）。结论：质量分数1% FCPs干预可能通过改善HFD小鼠肝脏氧化还原状态,促进肝脏脂肪分解代谢,起到减少小鼠肝脏脂肪蓄积和改善脂代谢。     

Inhibition of toxicogenic Bacillus licheniformis 553/1 in Nigerian Wara soft cheese by nisin-producing Lactococcus lactis LAC309

Wara soft cheese is a traditionally produced cheese in Nigeria. The production of this cheese includes a heating step for killing vegetative cells. Therefore, mainly spore-forming bacteria surviving the process may function as the first spoilers resulting in lowered shelf-life and safety of the product. In this study, we investigated if the addition of a nisin-producing Lactococcus lactis LAC309 starter after the high temperature treatment could result in nisin production and inhibition of the toxicogenic Bacillus licheniformis 553/1 strain spiked into the cheese. The results showed that L. lactis LAC309 could produce nisin in Wara cheese and that the strain inhibited (3 log reduction) B. licheniformis 553/1 in Wara cheese. Food technologists developing industrialised Wara cheese should therefore consider including a nisin-producing starter strain in the cheese-making process.