Breastfeeding anchors infant immunity and long-term health, but its benefits are threatened by Staphylococcus aureus (S. aureus) mastitis, an increasingly prevalent condition driven by antimicrobial resistance and therapeutic limitations. Beyond compromising maternal wellness, mastitis threatens the safety and continuity of breast milk, highlighting a critical need for innovative intervention strategies. Herein, we demonstrated that α‑ketobutyrate (α-KB), a metabolite of the transsulfuration pathway, mitigated S. aureus‑induced inflammation, oxidative stress, and blood-milk barrier (BMB) disruption both in vivo and in vitro. α‑KB enhanced macroautophagic/autophagic responses, marked by increased ATG5, BECN1 (beclin 1), and LC3-II:LC3-I conversion and reduced SQSTM1/p62, through a RIPK1-lactate-TFEB axis. Specifically, it directly bound and stabilized RIPK1, elevated lactate production, and drove TFEB nuclear translocation to activate macroautophagy/autophagy and promote intracellular bacterial clearance. Molecular docking and molecular dynamics simulations suggested stable α‑KB and RIPK1 binding via hydrophobic and hydrogen bond interactions; RIPK1 knockout abolished α‑KB-induced autophagy and lactate generation, effects rescued by lactate supplementation. This study identifies a novel immunometabolic circuit linking a metabolite to RIPK1-lactate-TFEB-mediated autophagy, offering therapeutic potential against antibiotic‑resistant S. aureus mastitis and presenting a new paradigm for safeguarding breastfeeding quality and infant health.Abbreviations: 3-MA: 3-methyladenine; α-KB: α‑ketobutyrate; ATG5: autophagy related 5; BMB: blood-milk barrier; CETSA: cellular thermal shift assay; DARTS: drug affinity responsive target stability; IL1B: interleukin 1 beta; IL6: interleukin 6; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MST: microscale thermophoresis; NOS2: nitric oxide synthase 2; OCLN: occludin; PBS: phosphate-buffered saline; PTGS2: prostaglandin-endoperoxide synthase 2; Rapa: rapamycin; RIPK1: receptor interacting serine/threonine kinase 1; RT-PCR: real-time polymerasechain reaction;S. aureus:Staphylococcus aureus; SEM: standard error of the mean; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TJP1: tight junction protein 1; TNF: tumor necrosis factor; WT: wild-type.

L-arginine, as an essential substance of the immune system, plays a vital role in innate immunity. MiR155, a multi-functional microRNA, has gained importance as a regulator of homeostasis in immune cells. However, the immunoregulatory mechanism between L-arginine and miR155 in bacterial infections is unknown. Here, we investigated the potential role of miR155 in inflammation and the molecular regulatory mechanisms of L-arginine in Streptococcus uberis (S. uberis) infections. And we observed that miR155 was up-regulated after infection, accompanying the depletion of L-arginine, leading to metabolic disorders of amino acids and severe tissue damage. Mechanically, the upregulated miR155 mediated by the p65 protein played a pro-inflammatory role by suppressing the suppressor of cytokine signaling 6 (SOCS6)-mediated p65 ubiquitination and degradation. This culminated in a violently inflammatory response and tissue damage. Interestingly, a significant anti-inflammatory effect was revealed in L-arginine supplementation by reducing miR155 production via inhibiting p65. This work firstly uncovers the pro-inflammatory role of miR155 and an anti-inflammatory mechanism of L-arginine in S.uberis infection with a mouse mastitis model. Collectively, we provide new insights and strategies for the prevention and control of this important pathogen, which is of great significance for ensuring human food health and safety.

AbstractBackgroundNuciferine (NUC), a natural compound extracted from lotus leaves, has been proven to have anti‐obesity effects. However, the development and application of NUC as an anti‐obesity drug in dogs are hindered due to its poor water solubility and low bioavailability.ObjectiveTo promote the development of NUC‐related products for anti‐obesity in dogs, this study prepared NUC into a liposome formulation and evaluated its characteristics, pharmacokinetics in dogs, and anti‐obesity effects on high‐fat diet dogs.MethodsNUC liposomes were prepared by the ethanol injection method, using NUC, egg lecithin, and β‐sitosterol as raw materials. The characteristics and release rate in vitro of liposomes were evaluated by particle size analyser and dialysis method, respectively. The pharmacokinetics in dogs after oral administration of NUC‐liposomes was carried out by the high‐performance liquid chromatography (HPLC) method. Moreover, we investigated the anti‐obesity effect of NUC‐liposomes on obese dogs fed with a high‐fat diet.ResultsNUC‐liposome was successfully prepared, with an EE of (79.31 ± 1.06)%, a particle size of (81.25 ± 3.14) nm, a zeta potential of (–18.75 ± 0.23) mV, and a PDI of 0.175 ± 0.031. The cumulative release rate in vitro of NUC from NUC‐liposomes was slower than that of NUC. The T1/2 and relative bioavailability of NUC‐liposomes in dogs increased, and CL reduced compared with NUC. In addition, the preventive effect of NUC‐liposomes on obesity in high‐fat diet dogs is stronger than that of NUC.ConclusionsThe liposome formulation of NUC was conducive to improve its relative bioavailability and anti‐obesity effect in dogs.

《动物病理学》是高职院校动物医学及宠物类等相关专业的专业基础课.本文中提出了"爱国敬业、辩证思维、社会责任、环保理念"的教育教学思政治体制系,并同时从课程目标、内容、教学方法等三个方面,介绍了该科目的思政教育课程设置,培养了学生良好的伦理观、价值观,以及社会责任心.课程设计为其他自然类课程思政教学提供了重要借鉴与参照.

The aim of this study was to investigate the mechanism of inulin with high degree of polymerization in improving high-fat diet-induced obesity in dogs based on the gut- adipose tissue axis. Forty poodle were randomly divided into five groups: common diet group， high-fat diet group， and low-dose， medium-dose and high-dose inulin with high degree of polymerization groups. Dogs in common diet group were fed with normal diet， and in high-fat diet were fed with high-fat diet. Dogs in low-dose， medium-dose and high-dose inulin with high degree of polymerization groups were fed with high-fat diet containing 1.0%， 3.0% and 5.0% inulin with high degree of polymerization， respectively. The test period was 12 weeks. After the experiment， the levels of serum glucose， fat， and inflammatory factors were measured， and the relative expressions of mRNA and protein of related factors in subcutaneous adipose tissue and colon mucosa were detected using real-time fluorescent PCR and western blot， respectively. The results showed as follows: Inulin with high degree of polymerization effectively reduced the body weight， body fat rate， and blood lipid level， meanwhile improve impaired glucose tolerance in dogs fed with high-fat diet. Moreover， inulin with high degree of polymerization increased the mRNA and protein expression of occludin and Zone-1in colonic mucosa， and reduced levels of serum lipopolysaccharide （LPS）， IL-6 and TNF-ɑ and the expression of IL-6 and TNF-ɑ in adipose tissue. In conclusion， inulin with high degree of polymerization can improve the obesity induced by high-fat diet in dogs， and Its mechanism may be related to the regulation of the gut-adipose tissue axis of "intestinal mucosal barrier function - LPS translocation - adipose tissue inflammation".

Abstract Background The antisense noncoding RNA in the INK4 locus (ANRIL) has been confirmed related to multiple disease progression, but the role and exact mechanisms of lnc‐ANRIL in lipopolysaccharide (LPS)‐induced inflammation of bovine mammary epithelial cells (MAC‐T) remain unclear. Aims This manuscript focused on expounding the functional role of lnc‐ANRIL through experiments performed in MAC‐T. Methods At the in vitro level, we established a Bovine mammary epithelial cell (BMEC) cell model of mastitis by LPS treatment. Transfection of siRNA was examined by immunofluorescence localization and RT‐qPCR. CCK8, clonogenic assay and EdU were used to detect the proliferation ability of the cells. Cell cycle and apoptosis were detected by flow cytometry and Western blot. The levels of inflammatory factors and oxidative stress markers were detected by ELISA kits. Results Cell Counting Kit‐8, colony formation, and 5‐ethynyl‐20‐deoxyuridine were adopted and the data illustrated that LPS could significantly suppress the cell proliferation, while knockdown of lnc‐ANRIL expression obviously promoted MAC‐T cell proliferation compared with LPS or LPS + si‐NC group. Flow cytometry analysis demonstrated that lnc‐ANRIL could induce MAC‐T cell apoptosis. In addition, downregulation of lnc‐ANRIL affected LPS‐induced immune response by regulating inflammatory factor expressions and modulating the nuclear factor kappa B (NF‐κB) axis in MAC‐T cells. Conclusion Our results suggest that lnc‐ANRIL is involved in the regulation of cell proliferation, cell cycle, and cell apoptosis of MAC‐T cells, and plays an important role in the inflammatory and immune response of MAC‐T cells through the regulation of the NF‐κB pathway, proposing new therapeutic strategies for the treatment of innate immune response‐related disease such as bovine mastitis.

Mastitis is a common disorder in women capable of altering the normal physiological function of the mammary gland. It has been reported that mammary epithelial cells (MECs) could be involved in treating mastitis by regulating the inflammatory response and miR-155 might participate in this process. However, the effects of MECs-derived exosomal miR-155-inhibitor in treating mastitis and the regarding mechanism are still unknown. In our study, mouse mammary epithelial cells (HC11) were applied to study the role of MECs-derived exosomal miR-155-inhibitor in the treatment of mastitis and explore the mechanism. Results in our study showed that specific markers including CD63 and Apo-A1 were expressed in blank exosomes and exosomes containing miR-155-inhibitor isolated from transfected HC11 cells. Results of immunofluorescence showed that the blank exosomes and exosomes (containing miR-155-inhibitor) labeled with PKH26 were absorbed in HC11 cells. The level of miR-155 was decreased obviously in Engineered exosomes with miR-155-inhibitor and HC11 cells Transfected with exosome containing miR-155-inhibitor. The level of miR-155 was increased and cell apoptosis was promoted obviously in HC11 cells induced by LPS, however, they were decreased obviously after transfecting with an exosome containing miR-155-inhibitor. The level of TLR2, TLR4, TLR6, NF-κB, TNF-α, and IL-1β was increased obviously in LPS-induced HC11 cells, however, they were decreased obviously after transfecting with an exosome containing miR-155-inhibitor. The change in IL-10 level is opposite to the above genes. Taken together, exosomal miR-155-inhibitor could decrease the apoptosis of MECs and inhibit the inflammatory response to treat mastitis by down-regulation in the TLRs/NF-κB signaling pathway, which might be a new therapeutic target for mastitis.

This study was to evaluate the anti-obesity effect and safety of nuciferine(NUC)on high-fat diet beagles.After 2 weeks of a-daptive feeding,a total of 36 adult beagles were used and randomly divided into 6 groups fed with normal diet,normal diet with 0.1％NUC,high fat diet with 0.05％NUC,high fat diet with 0.1％NUC,and high fat diet with 0.15％NUC,respectively.After 8 weeks of feeding,the tests of corpuscle,biochemistry and electrolyte in blood samples collected from the tested dogs were performed,and the subcutaneous adi-pose tissue of the groin was stained with H & E to observe the size of adipocytes.The results showed that the final body weight,body weight gain,subcutaneous fat thickness,adipocyte area,triglycerides(TG),total cholesterol(TC),and low-density lipoprotein cholesterol(LDL-C)in the high fat diet group were higher than those in the normal diet group,while supplementing 0.1％NUC and 0.15％NUC re-versed these changes.In addition,supplementation of 0.1％NUC reduced the levels of total bilirubin(TBIL)and alanine aminotransferase(ALT)in the high-fat diet dogs.Supplementation of different doses of NUC had no effect on corpuscle and serum electrolytes in the blood of the animals.In summary,NUC in the diet improved the obesity and liver enzymes induced by a high-fat diet in beagles,with a 0.1％added dose having the best effect.

本试验旨在探讨miR-142-5p对脂多糖(LPS)诱导的小鼠乳腺上皮细胞炎性因子释放以及增殖和凋亡的影响.采用小鼠乳腺上皮细胞系经LPS诱发炎症反应,分别经miR-142-5p模拟物或抑制剂处理,检测细胞TNF-α、IL-1 β、IL-6和IL-8的释放水平,AKT/p65信号通路关键蛋白磷酸化水平以及细胞增殖和凋亡水平.结果显示:与对照组比较,LPS组TNF-α、IL-6、IL-1β、IL-8分泌水平显著上调(P＜0.05),p-AKT和p-P65蛋白相对表达水平显著上调(P＜0.05),G0/G1期细胞比率上调,S期细胞比率降低,细胞增殖活力下降,细胞凋亡率显著增加(P＜0.05);与LPS组相比,LPS+抑制剂组上述检测数值变化减弱(P＜0.05),而LPS+模拟物组上述检测数值变化则进一步增强(P＜0.05),LPS+抑制剂阴性对照组和LPS+模拟物阴性对照组上述检测数值均无显著差异(P＞0.05).结果表明,miR-142-5p可能通过激活AKT/p65信号通路,促进炎性因子的分泌和释放,并抑制细胞增殖,促进细胞凋亡.

本试验旨在研究脂联素(APN)/脂联素受体1(AdipoR1)/腺苷酸激活蛋白激酶(AMPK)信号通路在银杏叶提取物改善高脂饮食诱导的肥胖犬脂质代谢及脂肪沉积中的作用.试验选取雄性成年泰迪型贵宾犬50只,适应性饲喂2周后分成对照组(A组,n=6)和高脂饲粮组(n=44).对照组饲喂基础饲粮,高脂饲粮组饲喂高脂饲粮(基础饲粮+25％猪油).饲喂8周后高脂饲粮组成功建立肥胖犬模型,筛选30只肥胖犬,等分成5组:高脂饲粮对照组(B组,n=6)、银杏叶提取物组(C组,n=6)、阴性siRNA(N?siRNA)对照组(D组,n=6)、APN?siRNA组(E组,n=6)和AdipoR1?siRNA组(F组,n=6).A组继续饲喂基础饲粮,其他各组继续饲喂高脂饲粮.C组、D组、E组和F组每天按50 mg/kg BW的剂量灌服银杏叶提取物,A组和B组灌服等量生理盐水.此外,D组、E组和F组在腹部皮下注射500μL siRNA,A组、B组和C组注射等体积生理盐水,每周3次.试验周期为4周.试验结束后,测量试验犬的体重及体脂率,测定血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL?C)、高密度脂蛋白胆固醇(HDL?C)及APN含量,苏木精-伊红(HE)染色观察脂肪细胞大小变化,分别用实时荧光定量PCR(qRT?PCR)法和Western blot法检测APN/AdipoR1/AMPK信号通路中相关分子基因表达和蛋白表达变化.结果显示:1)B组体重及体脂率显著高于A组与C组(P<0.05),C组体重及体脂率显著低于E组与F组(P<0.05).2)B组血清TG、TC、LDL?C及APN含量显著高于A组与C组(P<0.05),HDL?C含量显著低于A组与C组(P<0.05);C组血清TG、TC、LDL?C含量显著低于E组和F组(P<0.05),HDL?C含量高于E组和F组(P<0.05).3)C组和D组皮下脂肪组织中脂肪细胞面积显著小于B组、E组和F组(P<0.05).4)C组脂肪组织中APN的mRNA和蛋白相对表达量显著高于B组与E组(P<0.05),AdipoR1的mRNA和蛋白相对表达量显著高于B组与F组(P<0.05),腺苷单磷酸活化蛋白激酶α1(AMPKα1)的mRNA相对表达量和磷酸化腺苷单磷酸活化蛋白激酶α1(p?AMPKα1)的蛋白相对表达量显著高于B组、E组与F组(P<0.05).综上所述,银杏叶提取物可以降低肥胖犬的体重、体脂率和血脂水平,这与银杏叶提取物激活脂肪组织APN/AdipoR1/AMPK信号通路,改善脂肪细胞脂质代谢与脂肪沉积的作用有关.

文章旨在研究银杏叶提取物对高脂饮食诱导肥胖犬脂肪沉积及脂质代谢的影响,试验选取雄性成年泰迪型贵宾犬30只,等分成5组,分别为对照组(CD)、高脂饲粮组(HFD)、低剂量银杏叶提取物组(LGL)、中剂量银杏叶提取物组(MGL)和高剂量银杏叶提取物组(HGL).CD组饲喂普通饲粮,HFD组饲喂高脂饲料,各银杏叶提取物饮食组分别饲喂含1％、3％和5％银杏叶提取物的高脂饲料,试验为期8周.结果显示,与HFD组相比,MGL组和HGL组体重和体脂率显著降低(P<0.05);MGL组和HGL组血清TG、LDL-C含量降低,HDL-C升高(P<0.05);MGL组和HGL组脂肪细胞面积变小(P<0.05);MGL组和HGL组AMPKα1的mRNA表达量上调,SREBP-1、FAS及PPARγ的mRNA表达量下调;LGL组CTP-1蛋白表达量升高,FAS蛋白表达量降低,MGL组和HGL组AMPKα1及CPT-1蛋白表达量升高,ACC1、SREBP-1、FAS及PPARγ蛋白表达量降低.综上所述,银杏叶提取物具有促进肥胖犬脂质代谢,抑制脂肪沉积作用.

产学研协同创新育人对我国高职教育人才培养具有重大意义.以江苏农牧科技职业学院宠物专业为例,探讨高等职业院校宠物专业产学研协同创新育人平台的构建与实践.以产学研命运共同体建设为基础,将企业元素融入课程体系,最终形成"一个共同体、三大中心、四个核心团队"的产学研协同创新育人平台.实践表明,该平台能使多方共赢,对于推进校企合作及人才培养质量有着积极作用.

Based on the training needs of Pet Care and Training Major in higher vocational colleges, we reformed the original restrictions of teaching and research office and jointly built a modular teaching team by combining the major with school-enterprise cooperation. We set up course module, task module and content module based on the requirement of professional ability. Through the flexible combination of modules, it opens up a path for the integration of "position-courses-competition-certificates-Innovation". The teaching team should cooperate for the teaching task and will explore effective ways to promote the high-quality development of vocational education.

为探讨炎症小体NLRP3在大肠杆菌诱发的实验性大鼠乳腺炎中的作用,36只SD大鼠随机分为对照组、大肠杆菌组和抑制剂组.其中:大肠杆菌组于大鼠产后72h经乳头管注入2×1012CFU/mL大肠杆菌悬液100μL/侧到第4对乳腺(两侧)内;抑制剂组在注射大肠杆菌悬液前0.5 h腹腔注射500 mg/kg格列本脲;对照组注射等量灭菌生理盐水,注射后12 h收集血清及乳腺组织.结果:大肠杆菌诱发能显著提高乳腺组织NLRP3及衔接蛋白ASC和炎症相关蛋白激酶Caspase-1的表达,促进炎性细胞因子IL-1β 的释放,从而引起N-乙酰-β-D-氨基葡萄糖苷酶(NAGase)活性及丙二醛(MDA)水平的显著升高.NLRP3的抑制剂格列本脲预处理能抑制NLRP3及ASC和Caspase-1的表达,降低炎性细胞因子IL-1β的释放,下调NAGase的活性和MDA水平.可见NLRP3炎症小体的激活在大肠杆菌诱导的实验性乳腺炎症反应中发挥了重要的作用.

Inflammation induced by gut microbiota disorder plays an important role in promoting obesity. Inulin has beneficial effects on gut microflora and metabolic endotoxaemia. However, the chain length of inulin determines its different physiological effects. This study aimed to investigate the effect of low polymerization inulin (LPI) and high polymerization inulin (HPI) on inflammation in dogs with obesity induced by a high-fat diet and its potential mechanism. HPI, relative to LPI, significantly reduced the concentrations of LPS, IL-6 and TNF-α in serum and downregulated both the mRNA and protein expression of TLR4, NF-κB, TNF-α and IL-6 in adipose tissue. HPI and LPI intervention reduced adipose tissue fatty accumulation, which improved obesity. Supplementation with LPI and HPI increased gut microbiota diversity and altered specific bacterial populations at both the phylum and genus levels. The relative abundances of Prevotella, Fusobacterium and Enterobacter, which were positively correlated with the serum concentrations of LPS, IL-6 and TNF-α, were reduced. Our results demonstrate that both LPI and HPI can be used as an effective strategy for reducing inflammation and regulating gut microbiota, which can ameliorate obesity in dogs. Moreover, HPI exerts more positive regulation of the inflammatory response and gut microbiota dysfunction than LPI.

近年来,专业教学资源库的建设与研究正如火如荼地开展,截止目前教育部和财政部陆续批准了90多个高职教育专业教学资源库的立项,平均每个资源库建设都有10多所高职院校和10多家企业共同参与,优化整合专业优质资源,提高教学质量.

信息化时代使线上与线下混合式教学得以顺利实施,线上学习具有众多优点,线上线下混合式教学是现代教育的发展趋势.以中国大学MOOC平台开展的"小动物影像技术"线上线下混合式教学为例,阐述了线上线下混合式教学的方法与体会.

本试验旨在评估不同蛋白质水平饲粮对肥胖犬体况、血清生化指标、粪便短链脂肪酸浓度及肠道菌群结构的影响.选取30只肥胖型拉布拉多猎犬,随机等分为3组:低蛋白质组(LP组),饲喂粗蛋白质含量为20.58％的低蛋白质饲粮;中蛋白质组(MP组),饲喂粗蛋白质含量为27.77％的中蛋白质饲粮;高蛋白质组(HP组),饲喂粗蛋白质含量为39.04％的高蛋白质饲粮).试验期为45 d.结果表明:1)与LP组和MP组比较,HP组犬体重、体脂率以及血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)含量显著降低(P＜0.05).2)与LP组和MP组比较,HP组粪便中乙酸及总短链脂肪酸浓度显著或极显著降低(P＜0.05或P＜0.01),丁酸浓度显著升高(P＜0.05);体脂率与粪便中乙酸及总短链脂肪酸浓度呈正相关关系,与丁酸浓度呈负相关关系.3)与LP组和MP组比较,HP组肠道菌群Simpson指数显著升高(P＜0.05),厚壁菌门相对丰度显著升高(P＜0.05),拟杆菌门相对丰度显著降低(P＜0.05),拟杆菌门/厚壁菌门比值显著降低(P＜0.05);在属水平,HP组主要富集梭菌属、瘤胃球菌属及普拉梭菌属等细菌;HP组肠道菌群基因功能主要富集在黄酮和黄酮醇生物合成、色氨酸代谢及柠檬烯和蒎烯降解等7个第3层级KEGG通路上.综上所述,高蛋白质饲粮可改善肥胖犬肠道菌群结构及短链脂肪酸代谢,有减重降脂作用.

Bovine mastitis is a threat to the health of the dairy cow. MicroRNAs (miRs) serve an important role in the progression of bovine mastitis, regulating immune and defense responses. The present study aimed to investigate the possible effects and mechanisms of bovine mastitis underlying miR-142-5p and Bcl-2 associated athanogene 5 (BAG5) in in vitro lipopolysaccharide (LPS)-induced models. Reverse transcription-quantitative PCR and western blotting were performed to determine mRNA and protein expression levels, respectively. ELISAs were conducted to assess the levels of cytokines and an immunofluorescence assay was performed to determine the expression of BAG5. Cell Counting Kit-8, clone formation and 5-ethynyl-2'-deoxyuridine assays were conducted to determine cell viability and proliferation of bovine mammary epithelial MAC-T cells, respectively. Flow cytometry was performed to measure MAC-T cell cycle distribution and apoptosis, and a luciferase assay was conducted to verify whether BAG5 was a target of miR-142-5p. The results indicated that miR-142-5p was upregulated in MAC-T cells treated with LPS compared with the control group. miR-142-5p mimics transfection significantly activated the cytokines TNF-α, IL-1β, IL-6 and IL-8, and significantly increased the expression levels of NF-κB signaling pathway-related proteins in LPS-treated cells. The luciferase activity of MAC-T cells treated with miR-142-5p mimics and BAG5 3'untranslated region wild type decreased, compared with mutant type. By contrast, BAG5 overexpression significantly downregulated the levels of cytokines, including TNF-α, IL-1β, IL-6 and IL-8, in LPS-treated cells. BAG5 overexpression significantly promoted cell proliferation and viability, decreased apoptosis, and regulated Caspase-3, Caspase-9, Bcl-2 and Bax expression in LPS-treated MAC-T cells, which was significantly reversed by transfection with miR-142-5p mimics. In conclusion, the results of the present study suggested that miR-142-5p may promote the progression of bovine mastitis via targeting BAG5. Therefore, the present study provided the foundations for future investigations.

本研究旨在评估短链脂肪酸在慢性肾衰竭患犬和健康犬中的水平,探究短链脂肪酸变化的原因及其对肾功能的影响.选取22例轻度慢性肾衰患犬(M-CRF组)、29例重度慢性肾衰患犬(S-CRF组)和26例健康对照犬(HC组),用16S rDNA测序技术分析肠道菌群多样性,气相色谱法检测粪中短链脂肪酸浓度.通过粪菌移植和补充丁酸钠给5/6肾摘除犬,观察肠道菌群及丁酸钠对肾功能影响.结果 显示:1)S-CRF组肠道菌群多样性指标观察物种数及Simpson指数低于HC组(P＜0.05),PCoA分析显示,S-CRF组肠道菌群与M-CRF、HC组有差异.2) LEfSe分析显示,S-CRF组和HC组间大量差异菌群,拟杆菌科、拟杆菌属及假单胞菌科等7个菌种富集于S-CRF组,普氏杆菌科、梭菌科、普氏杆菌属及普拉梭菌属等11个菌种富集于HC组.CCA分析发现富集于S-CRF组菌种丰度与肾功能指标呈正相关.3)S-CRF组粪中乙酸、丙酸及丁酸浓度均显著低于HC组和M-CRF组,M-CRF组丁酸浓度显著低于HC组(P＜0.05),且丁酸浓度与血中胱抑素C(Cys-c)、肌酐(Cr)及尿素氮(BUN)等肾功能指标呈负相关(r值分别为-0.451、-0.583和-0.514,P＜0.01).4)与慢性肾衰模型组(5/6 Nx组)比较,慢性肾衰犬给与丁酸钠8周后,血清Cr和BUN显著降低(P＜0.05);粪菌移植8周后,血清Cr和BUN显著升高(P＜0.05),丁酸钠可回调血清Cr和BUN水平.综上表明,慢性肾衰竭患犬肠道菌群多样性降低,菌群结构及丰度改变,粪中短链脂肪酸浓度降低,这些变化可加剧肾功能障碍.为犬慢性肾衰竭的防治提供新的理论依据.