铁皮石斛多糖对高脂饮食小鼠肠黏膜结构及菌群的影响

为考察铁皮石斛多糖对高脂饮食小鼠肠黏膜屏障的影响,采用水提醇沉法提取铁皮石斛多糖,联合高脂饲料给予小鼠8周后观察肠黏膜结构及肠黏膜菌群的变化。结果显示高脂饮食显著破坏了肠黏膜结构,表现为肠黏膜萎缩,上皮细胞脱落并伴有炎性渗出,Corynebacterium_1及Staphylococcus等与感染及炎症相关的菌属大量增殖。铁皮石斛多糖对肠黏膜结构有较好的保护作用,并可减少Corynebacterium_1的丰度,同时提高肠黏膜共生菌Candidatus_Arthromitus的丰度,促进了Muribaculaceae、Bacteroides、Lachnospiraceae_NK4A136_group等碳水化合物代谢、短链脂肪酸产生相关菌的增殖。研究表明铁皮石斛多糖对肠黏膜屏障的保护作用或与其维持肠黏膜结构完整,调节肠黏膜菌群组成及促进碳水化合物代谢,生成短链脂肪酸有关。     

高脂饮食中添加短链菊粉对小鼠肠道菌群的影响

目的:探究高脂饮食中添加短链菊粉对小鼠肠道菌群的影响。方法:选择8周龄雄性小鼠,5只喂食高脂饲料,5只喂食10%菊粉复合型高脂饲料,喂食8周后收集小鼠粪便,检测小鼠粪便中三种主要的短链脂肪酸。同时,提取小鼠粪便中的细菌基因组,对菌群基因组16S rRNA基因V4高变区进行测序,对数据进行PCoA分析、Alpha多样性分析、LEfSe分析和16S功能预测。结果:菊粉添加后,小鼠粪便中含有的细菌DNA量增多,短链脂肪酸增加。菊粉组和对照组PCoA图可以看到明显聚类。菊粉组物种多样性低于对照组。菊粉组小鼠粪便中S24_7菌科丰度上升;Lachnospiraceae(毛螺菌科),Ruminococcaceae(瘤胃菌科)和Deferribacteraceae(脱铁杆菌科)丰度下降。16S基因功能预测发现22个第二层级的KEGG通路发生变化。结论:高脂饮食情况下短链菊粉的添加会改变小鼠肠道菌群,继而影响肠道菌群的功能。     

基于肠道菌群和短链脂肪酸代谢探讨不同饮食条件下高脂血症大鼠发病机制

目的 本研究拟对比两种不同高脂饮食方式诱导的高脂血症大鼠肠道菌群变化与短链脂肪酸代谢特征,以宿主-肠道菌群-代谢角度探讨高脂血症可能的微观机制。方法 SPF级SD大鼠分为：正常饮食组(CG组):饲喂大鼠维持饲料;高脂饮食组(HFD1组):每天足量饲喂高脂饲料;限饲高脂饮食组(HFD2组):每天限量饲喂高脂饲料80 g,不限量饲喂维持饲料。8周后检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平;苏木精-伊红(HE)染色观察大鼠肝组织和肾周脂肪病理学变化;取结肠内容物进行16S rDNA高通量测序,观察肠道菌群结构与功能的变化,并检测结肠内容物中短链脂肪酸的含量。结果 与CG组相比,HFD1组和HFD2组大鼠摄食量下降,体重升高;血清中TC、TG、LDL-C均显著升高;肝组织发生明显脂肪变性,肾周脂肪出现炎性病变;高脂干预后大鼠肠道菌群相对丰度显著变化,其中乳杆菌属相对丰度明显降低,菌群结构和功能变化明显,总短链脂肪酸、乙酸、丁酸、异丁酸下降显著。结论 两种高脂饮食方式均能引起大鼠高脂血症,且发病机制基本一致,均与脂质代谢以...     

铁皮石斛对脾虚便秘小鼠肠道菌群多样性的影响

探讨铁皮石斛对脾虚便秘小鼠肠道菌群的影响,为铁皮石斛对脾虚便秘的疗效机制及临床组方提供依据。

选取12只SPF级昆明小鼠随机分为正常组、模型组、铁皮石斛组和枳术汤组,每组3只。造模阶段正常组灌胃无菌水,模型组和治疗组采用番泻叶水煎液灌胃7 d后,限制饮食饮水8 d,建立脾虚便秘模型。造模成功后,正常组和模型组灌胃无菌水,治疗组分别以铁皮石斛和枳术汤水煎液干预5 d。治疗结束后,收集各组小鼠盲肠内容物样本进行16S rDNA高通量测序。

脾虚便秘小鼠排便量减少,粪便细小,干燥,质硬,呈黄色。铁皮石斛和枳术汤分别治疗后,小鼠排便量增加,粪便软硬适中,呈黑褐色。测序分析发现,正常组与铁皮石斛组的共有OTU数最多,与枳术汤组的共有OTU数最少。α−多样性指数与PCA结果表明,铁皮石斛组菌属结构较其余两组更接近正常组小鼠。物种相对丰度及组成结果表明,铁皮石斛增加了脾虚便秘小鼠双歧杆菌属相对丰度,抑制了乳杆菌属、拟杆菌属相对丰度,但对菌群丰度的调节作用不及枳术汤;LEfSe分析与随机森林分析鉴定出布劳特菌属和活泼瘤胃球菌是铁皮石斛组与其他组别的差异菌群。

铁皮石斛能恢复脾虚便秘小鼠肠道菌群的多样性,可调节肠道菌群相对丰度,布劳特菌属和活泼瘤胃球菌可能是铁皮石斛干预脾虚便秘小鼠的肠道关键指示菌。

     

广叶绣球菌多糖对免疫低下小鼠肠道免疫功能的调节作用

通过研究广叶绣球菌多糖对免疫低下小鼠肠道菌群、细胞因子表达量及短链脂肪酸的影响,探究广叶绣球菌多糖的免疫作用机制。腹腔注射环磷酰胺构建免疫低下小鼠模型,将小鼠分为6组：正常对照组、模型组、广叶绣球菌多糖低、中、高剂量组以及阳性对照组,连续饲养30d后处死取样,HE染色观察小肠组织结构,酶联免疫吸附法测定小肠白细胞介素-6（IL-6）、IL-10、肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）的表达水平,高通量测序技术分析小鼠肠道菌群的变化,气-质联用（GC-MS）技术分析盲肠内容物短链脂肪酸（SCFAs）的含量。结果表明,广叶绣球菌多糖高剂量组可显著改善绒毛肿胀和变短现象,提高绒毛长度/隐窝深度的比值（V/C值）和小肠IL-6、IL-10、TNF-α、IFN-γ细胞因子含量（P<0.05或P<0.01）,提高拟杆菌属Bacteroides、拟普雷沃菌属Alloprevotella、丁酸弧菌属Butyrivibrio、Intestinimonas、链球菌属Streptococcus的相对丰度（P<0.05或P<0.01）;各剂量组均可提高盲肠内6种主要短链脂肪酸含量,差异达显著或极显著水平（P<0.05或P<0.01）。试验组与阳性对照组趋势一致。广叶绣球菌多糖可通过改善免疫低下小鼠的肠道粘膜形态,提高小肠细胞因子水平,调节肠道菌群结构,增加SCFAs产生菌的相对丰度,提高短链脂肪酸含量,调节免疫低下小鼠的肠道免疫功能。     

短链脂肪酸对肠黏膜屏障的影响

肠黏膜屏障具有将致病性抗原等肠内物质与内环境隔离的功能,以维持内环境的相对稳定和机体的正常生命活动。其功能的维持依赖于人肠黏膜上皮细胞、肠道内正常菌群、肠道内分泌物和肠相关免疫细胞之间的功能协调,而其功能的发挥又受体内许多信号分子的影响。短链脂肪酸（short-chain fatty acids,SCFAs）就是其中一种重要的信号分子。SCFAs是肠道菌群的主要代谢产物之一,是肠道菌群与宿主代谢相互作用的媒介。宿主体内的SCFAs主要来自肠道菌群对膳食纤维的酵解,越来越多的研究证实,SCFAs不仅可以被肠道菌群利用,还可调节肠黏膜屏障及多种组织器官的代谢。本文主要就SCFAs对肠黏膜屏障的影响进行综述。

     

高脂饮食诱导肠道微生物代谢产物短链脂肪酸改变进而影响食物过敏的发生

通过回顾过敏性疾病以及高脂饮食、肥胖等的大量研究报告,探究高脂饮食以及高脂饮食带来的肥胖是否会对食物过敏的发生产生影响以及可能的机制。研究发现,高脂饮食可能会增加食物过敏发生率,降低食物过敏阈值,增加食物过敏的风险,并且高脂饮食对肠道微生物的影响是其中的一个原因。高脂饮食改变肠道微生物结构,导致短链脂肪酸产生差异,而短链脂肪酸通过G蛋白偶联受体、组蛋白乙酰化等途径引起Treg细胞分化、IgA产生以及致耐受性的DC细胞产生,影响肠道屏障的健康,因此,高脂饮食对肠道微生物结构的改变带来的短链脂肪酸的产生差异影响了肠道屏障的健康,进而导致食物过敏的阈值降低,易感性增加。     

哺乳动物肠道微生物与碳水化合物的互作及其影响

肠道微生物具有调节宿主营养、免疫以及能量代谢等生理功能。饮食是影响哺乳动物的肠道微生物的一个重要因素。碳水化合物是哺乳动物食物能量的主要来源,因此研究肠道微生物与碳水化合物的代谢之间的关系及其影响具有重要意义。基于近年相关研究,本文从碳水化合物对肠道微生物组成的影响、肠道微生物对碳水化合物的代谢机制以及碳水化合物发酵产物短链脂肪酸对宿主的影响3个方面进行了综述。研究表明,肠道微生物可用于发酵的碳水化合物类型主要是抗性淀粉和非淀粉多糖;不同类型的碳水化合物会导致肠道菌群发生适应性变化;复杂多糖发酵产生的短链脂肪酸在调节宿主能量平衡和免疫应答方面发挥了重要作用。总结近年来相关研究,可加深对肠道菌群对宿主碳水化合物代谢贡献的理解,为哺乳动物机体健康状况的营养调控策略提供参考。     

绿豆对高脂饮食大鼠肠道微生物及脂代谢调节的影响

本文研究并评估了绿豆对高脂饮食大鼠血脂代谢(TG、TC、LDL-C、HDL-C)、肝脏脂质分布、抗氧化酶活性(SOD、CAT、T-AOC)的影响。还研究了绿豆对高脂饮食大鼠肠道微生物菌群及短链脂肪酸(SCFAs)的调节作用。结果表明,与高脂饮食组相比,添加绿豆显著减轻大鼠了血清和肝脏的脂质积累,并提高了抗氧化酶的活性。大鼠盲肠中的SCFAs含量随绿豆剂量的增加而增加。大鼠盲肠内容物以厚壁菌和拟杆菌为主。绿豆摄入影响了大鼠肠道微生物群的丰度,拟杆菌和放线菌相对丰度等增加。这些结果表明,绿豆具有改善肠道微生物及调节脂代谢的作用,对机体有显著的保护作用。     

红花多糖对肠道微生态失调小鼠肠黏膜sIgA、血浆内毒素和肠道菌群的影响

目的 研究红花多糖对肠道微生态失调小鼠的调节作用,探讨红花多糖改善微生态失调与肠黏膜免疫、血浆内毒素及肠道菌群的关系。 方法 应用盐酸林可霉素灌胃建立肠道微生态失调小鼠模型,然后用红花多糖进行治疗,同时设正常对照组(n=5)、自然恢复组(n=5)和丽珠肠乐组(n=5)。于给药7 d后处死小鼠,进行肠黏膜sIgA、血浆内毒素的检测,以及采用16S rRNA测序技术,对肠道菌群进行群落结构和多样性分析。 结果 给药治疗后,小鼠肠黏膜sIgA水平升高(F=3.990 0,P=0.009 0),血浆内毒素水平降低(F=3.866 0,P=0.010 0);基因测序结果显示红花多糖组和丽珠肠乐组菌群丰度与多样性均有提升,并能显著增加小鼠肠道菌群中毛螺菌属(t=2.602 8,P=0.009 2)、粪球菌属(t=4.551 0,P结论 红花多糖可能通过提高小鼠肠黏膜sIgA含量,抑制血浆内毒素含量并通过增加肠道有益菌、降低致病菌、部分恢复和改善肠道菌群而发挥对微生态失调小鼠肠道菌群结构的调整作用。     

Targeting the gut microbiota with resveratrol: a demonstration of novel evidence for the management of hepatic steatosis

Resveratrol is a natural polyphenol that has been reported to reduce the risk of obesity and nonalcoholic fatty liver disease (NAFLD). Recent evidence has demonstrated that the gut microbiota plays an important role in the protection against NAFLD and other metabolic diseases. The present study aimed to investigate the relationship between the gut microbiota and the beneficial effects of resveratrol on the amelioration of NAFLD in mice. We observed marked decreases in body weight and liver steatosis and improved insulin resistance in high-fat diet (HFD)-fed mice treated with resveratrol. Furthermore, we found that resveratrol treatment alleviated NAFLD in HFD-fed mice by improving the intestinal microenvironment, including gut barrier function and gut microbiota composition. On the one hand, resveratrol improved gut intestinal barrier integrity through the repair of intestinal mucosal morphology and increased the expression of physical barrier- and physiochemical barrier-related factors in HFD-fed mice. On the other hand, in HFD-fed mice, resveratrol supplementation modulated the gut bacterial composition. The resveratrol-induced gut microbiota was characterized by a decreased abundance of harmful bacteria, including Desulfovibrio, Lachnospiraceae_NK4A316_group and Alistipes, as well as an increased abundance of short-chain fatty acid (SCFA)-producing bacteria, such as Allobaculum, Bacteroides and Blautia. Moreover, transplantation of the HFDR-microbiota into HFD-fed mice sufficiently decreased body weight, liver steatosis and low-grade inflammation and improved hepatic lipid metabolism. Collectively, resveratrol would provide a potentially dietary intervention strategy against NAFLD through modulating the intestinal microenvironment.     

双歧杆菌三联活菌对肥胖小鼠的改善作用及其机制

探讨双歧杆菌三联活菌对高脂饮食诱导的肥胖小鼠的改善作用及其机制。

将24只LDLR^－/－小鼠随机分为正常组（n = 8,普通饲料,灌胃生理盐水）、高脂组（n = 8,高脂饲料,灌胃生理盐水）和干预组（n = 8,高脂饲料,灌胃双歧杆菌三联活菌）。所有小鼠均干预16周,每2周记录小鼠体质量,第15周进行口服葡萄糖耐量试验。小鼠处死后,检测血清中脂质和胰岛素指标;采用RT-PCR分析回肠中炎症因子和肠道紧密连接蛋白ZO-1、Occludin的mRNA相对表达量;采用HE染色评估回肠组织病理变化;采用16S rDNA高通量测序分析小鼠肠道微生物群变化特点。

与正常组相比,高脂组小鼠表现出明显的体质量增加、糖脂代谢紊乱、回肠炎症水平增加和肠道微生物群紊乱。干预后,干预组小鼠体质量下降,糖脂代谢紊乱改善,回肠炎症因子TLR4和TNF-α相对表达量显著下降（均P＜0.05）;而肠道紧密连接蛋白ZO-1和Occludin相对表达量显著增加（均P＜0.05）。测序结果表明,干预组小鼠肠道菌群中Firmicutes和Bifidobacterium丰度增加。

双歧杆菌三联活菌可能通过优化肥胖小鼠的肠道微生物群结构,增加Firmicutes和Bifidobacterium丰度,进而减轻肥胖小鼠体质量,调节糖脂代谢,降低肠道内炎症和修复肠黏膜屏障。

     

高脂食物对动脉硬化合并类风湿关节炎小鼠肠道菌群的影响

目的 分析高脂食物对动脉硬化合并类风湿关节炎小鼠肠道微生物的影响,了解动脉硬化合并类风湿关节炎小鼠肠道微生物的变化。方法 8周龄ApoE-/-小鼠饲喂高脂食物和普通食物至17周龄来诱发动脉硬化症状,再通过给17周龄ApoE-/-小鼠腹腔注射抗6-磷酸葡萄糖异构酶（glucose-6-phosphate isomerase,GPI）抗体呈阳性的K/BxN血清,从而诱导其产生类风湿关节炎症状。通过Illumina HiSeq平台对各组小鼠粪便进行16S rDNA V4区测序,分析动脉硬化合并类风湿关节炎小鼠肠道微生物的变化。结果 ApoE-/-小鼠饲喂高脂食物后,其血清低密度脂蛋白胆固醇（LDL-C）浓度和血清总胆固醇（TC）浓度均显著升高,主动脉内膜斑块面积比喂普通食物的ApoE-/-小鼠显著增加,表明ApoE-/-小鼠饲喂高脂食物后引起更显著的动脉硬化症状。再通过腹腔注射抗GPI抗体呈阳性的K/BxN血清,各组ApoE-/-小鼠均出现关节肿胀,饲喂高脂食物的ApoE-/-小鼠其踝关节宽度和临床评分（clinical score）低于饲喂普通食物组小鼠。OTU数、Shannon指数和Simpson指数显示高脂食物和K/BxN血清处理组ApoE-/-小鼠肠道菌群多样性降低,Firmicutes/Bacteroidetes值升高,t-test分析显示在属水平上,Prevotellaceae_UCG-001显著降低,Ruminiclostridium_6显著升高。t-test分析和Firmicutes/Bacteroidetes比值显示ApoE-/-小鼠肠道菌群结构紊乱。结论 高脂食物使ApoE-/-小鼠的肠道菌群组成和结构发生改变,导致ApoE-/-小鼠的动脉硬化症状加重,类风湿关节炎症状减轻。提示肠道微生物组成和结构的改变,可能与动脉硬化合并类风湿关节炎发病机制相关。     

A high-fat diet and high-fat and high-cholesterol diet may affect glucose and lipid metabolism differentially through gut microbiota in mice

This study was conducted to investigate the effects of a high-fat diet (HFD) and high-fat and high-cholesterol diet (HFHCD) on glucose and lipid metabolism and on the intestinal microbiota of the host animal. A total of 30 four-week-old female C57BL/6 mice were randomly divided into three groups (n=10) and fed with a normal diet (ND), HFD, or HFHCD for 12 weeks, respectively. The HFD significantly increased body weight and visceral adipose accumulation and partly lowered oral glucose tolerance compared with the ND and HFHCD. The HFHCD increased liver weight, liver fat infiltration, liver triglycerides, and liver total cholesterol compared with the ND and HFD. Moreover, it increased serum high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and total cholesterol compared with the ND and HFD and upregulated alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase significantly. The HFHCD also significantly decreased the α-diversity of the fecal bacteria of the mice, to a greater extent than the HFD. The composition of fecal bacteria among the three groups was apparently different. Compared with the HFHCD-fed mice, the HFD-fed mice had more Oscillospira, Odoribacter, Bacteroides, and [Prevotella], but less [Ruminococcus] and Akkermansia. Cecal short-chain fatty acids were significantly decreased after the mice were fed the HFD or HFHCD for 12 weeks. Our findings indicate that an HFD and HFHCD can alter the glucose and lipid metabolism of the host animal differentially; modifications of intestinal microbiota and their metabolites may be an important underlying mechanism.     

Effect of non-digestible gluco-oligosaccharides on glucose sensitivity in high fat diet fed mice

Non digestible dietary carbohydrates have been reported to modify lipaemia and post-prandial glycaemia and insulinaemia. The aim of this study was to investigate the effect of a non-digestible gluco-oligosaccharides (GOS) diet on glucose, insulin, triglycerides and free fatty acid blood levels and glucose sensitivity in high fat diet fed mice (a high fat diet composed of 45% fat, 35% carbohydrate and 20% protein). Female C57B16/J mice were divided into two groups fed a high fat diet (HF) for 20 weeks supplemented or not with 1.5 g/kg/day of GOS (HF-GOS). The GOS supplementation did not change body weight nor fat pad mass, nor any of the blood parameters measured (glucose, insulin, leptin, triglycerides, and free fatty acids). However, mice which received the GOS supplemented diet showed an increased glucose utilization after a 1 g/kg load of glucose compared with the mice fed the high fat diet alone. Our results suggest a role for non-digestible GOS in the regulation of carbohydrate metabolism.     

Short-Chain Fructo-Oligosaccharides Modulate Intestinal Microbiota and Metabolic Parameters of Humanized Gnotobiotic Diet Induced Obesity Mice

Prebiotic fibres like short-chain fructo-oligosaccharides (scFOS) are known to selectively modulate the composition of the intestinal microbiota and especially to stimulate Bifidobacteria. In parallel, the involvement of intestinal microbiota in host metabolic regulation has been recently highlighted. The objective of the study was to evaluate the effect of scFOS on the composition of the faecal microbiota and on metabolic parameters in an animal model of diet-induced obesity harbouring a human-type microbiota. Forty eight axenic C57BL/6J mice were inoculated with a sample of faecal human microbiota and randomly assigned to one of 3 diets for 7 weeks: a control diet, a high fat diet (HF, 60% of energy derived from fat)) or an isocaloric HF diet containing 10% of scFOS (HF-scFOS). Mice fed with the two HF gained at least 21% more weight than mice from the control group. Addition of scFOS partially abolished the deposition of fat mass but significantly increased the weight of the caecum. The analysis of the taxonomic composition of the faecal microbiota by FISH technique revealed that the addition of scFOS induced a significant increase of faecal Bifidobacteria and the Clostridium coccoides group whereas it decreased the Clostridium leptum group. In addition to modifying the composition of the faecal microbiota, scFOS most prominently affected the faecal metabolome (e.g. bile acids derivatives, hydroxyl monoenoic fatty acids) as well as urine, plasma hydrophilic and plasma lipid metabolomes. The increase in C. coccoides and the decrease in C. leptum, were highly correlated to these metabolic changes, including insulinaemia, as well as to the weight of the caecum (empty and full) but not the increase in Bifidobacteria. In conclusion scFOS induce profound metabolic changes by modulating the composition and the activity of the intestinal microbiota, that may partly explain their effect on the reduction of insulinaemia.     

益生菌干预对高脂高糖饮食诱导肥胖小鼠肠道菌群及脂代谢影响的研究

目的 探讨益生菌干预对高脂高糖饮食诱导肥胖小鼠肠道菌群及脂代谢的影响。方法 C57BL/6J雌性小鼠30只随机分为正常对照组、肥胖组和益生菌干预组,每组10只,分别给予标准饲料、高脂高糖饲料以及高脂高糖饲料同时给予益生菌干预,连续喂养6周,测量并分析三组小鼠的体重。留取小鼠粪便样本,应用PCR-DGGE法分析菌群,应用酶反应比色法分析三组小鼠血脂情况。结果 与正常对照组小鼠相比,肥胖小鼠体重明显增加,益生菌干预组小鼠体重略有增加;肥胖组小鼠肠道菌群紊乱,与正常对照组分别聚为两大类,益生菌干预组小鼠肠道菌群与正常对照组聚为一大类。肥胖小鼠血清总胆固醇、低密度脂蛋白含量升高,益生菌干预组小鼠较肥胖组血清总胆固醇、低密度脂蛋白含量降低,但与正常对照组仍有差异。结论 高脂高糖饮食诱导肥胖小鼠存在肠道菌群结构失调及脂代谢异常,益生菌干预可以改善肥胖小鼠菌群失调以及脂代谢紊乱。     

地衣芽胞杆菌BL63516对抗生素诱导的菌群紊乱小鼠肠黏膜屏障功能的影响

目的 探索地衣芽胞杆菌BL63516对肠道菌群和肠黏膜屏障功能调节的效果和可能机制,为临床疾病的治疗提供新思路。方法 采用健康清洁级雄性BALB/C小鼠30只构建动物模型,将小鼠分为3组（每组10只）,分别为对照组（CON组）、头孢曲松钠灌胃组（CS组）和地衣芽胞杆菌BL63516治疗组（BL组）,除CON组外其余两组小鼠给予300 mg/mL头孢曲松钠0.2 mL,2次/d灌服8 d,短期大量服用抗生素以建立肠道菌群紊乱模型。第9天起BL组小鼠给予地衣芽胞杆菌干预连续8 d。第17天摘眼球处死小鼠,取血、结肠、粪便样本。ELISA方法检测小鼠血清及肝脏组织中的细胞因子及LPS水平。PCR-变性梯度凝胶电泳方法及16S rRNA高通量测序测定小鼠肠道菌群结构。结果 地衣芽胞杆菌干预后小鼠血清LPS水平较模型组显著降低,屏障功能改善。且地衣芽胞杆菌治疗后BL组肠道菌群丰富度和多样性显著升高,菌群结构有所改变。结论 实验结果提示地衣芽胞杆菌BL63516可以有效改善抗生素所致的小鼠肠道菌群失调,对肠屏障功能有一定调节作用。