Effects of fish meal replacement by low‐gossypol cottonseed meal on growth performance,digestive enzyme activity,intestine histology and inflammatory gene expression of silver sillago (Sillago sihama Forsskál) (1775)

A 56‐day feeding trial was conducted to evaluate the effects on the growth performance, digestive enzyme activity, inflammatory genes expression and intestine histology of silver sillago, Sillago sihama (Forsskål 1775), by replacing fish meal (FM) with low‐gossypol cottonseed meal (LCSM). Five isonitrogenous and isolipidic diets were formulated, including R0 group (control, containing 550.0 g/kg FM), R16 group (88.5 g/kg LCSM and 461.5 g/kg FM), R32 group (177.0 g/kg LCSM and 373.0 g/kg FM), R48 group (265.5 g/kg LCSM and 284.5 g/kg FM) and R64 group (354.0 g/kg LCSM and 196.0 g/kg FM). Fish fed R0 and R16 groups had a significantly higher weight gain rate (WGR) and specific growth rate (SGR) than R48 and R64 groups (p < .05). In contrast to whole‐body crude protein, whole‐body moisture increased with the FM level of substitution (p < .05). With the increased amount of LCSM in the diet, the activity of intestinal amylase (AMS) increased significantly (p < .05), and intestinal trypsin (TRP) decreased (p < .05). Dietary LCSM substitution upregulated the expression of intestinal tumour necrosis factor‐α (TNF‐α), the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), and interleukin one beta (IL‐1β), but downregulated tight junction proteins ZO‐1(ZO‐1), transforming growth factor beta‐3 (TGF‐β3) and interleukin 10 (IL‐10) expression. Histological analysis revealed progressive morphological damage to the mid‐intestine with higher levels of FM replacement. These results showed that 88.5 g/kg (16%) of FM replaced by LCSM with amino acids (methionine and lysine) supplementation did not significantly reduce growth compared with FM‐based control.     

Effects of dietary sodium butyrate on growth,diet conversion,body chemical compositions and distal intestinal health in yellow drum (Nibea albiflora,Richardson)

The present study was conducted to investigate the effects of sodium butyrate (SB) on the physical barrier function, pro‐inflammatory response and possible underlying mechanisms in the distal intestine (DI) of yellow drum when fed a high‐SBM diet. Three iso‐proteic and iso‐lipidic diets were formulated with fish meal (FM, the control), 45% fish meal protein replaced by SBM (SBM) and 45% fish meal protein replaced by SBM but supplemented with 0.15% SB (SBM + SB). Fish were fed twice daily for 10 weeks. Results indicated that SB supplementation significantly increased the specific growth rate (SGR) and feed efficiency ratio (FER) and methionine content of muscle when compared with those of fish fed the SBM diet (p < .05). The morphologic histology results showed that SB dramatically improved the physical barrier structure, characterized as increases of fold height (FH) and muscular thickness (MT) (p < .05). RT‐qPCR data were accordant with morphologic histology results, in which claudin 3, claudin 4 and occludin were increased while claudin 7 and myosin light chain kinase (MLCK) mRNA expression levels were decreased (p < .05). Sodium butyrate also exerted anti‐inflammatory function, which may be attributed to the suppression of nucleus p65 protein expression. Results suggest SB can be incorporated in high‐SBM diets to ameliorate the negative consequences of alternative dietary ingredients on yellow drum physiology.     

一株大黄鱼致病性溶藻弧菌的耐药性及耐药基因分析

对一株分离自大黄鱼的致病性溶藻弧菌进行耐药性分析,分别用纸片扩散法、倍比稀释法检测了该菌对磺胺甲噁唑、氟苯尼考、盐酸多西环素、红霉素、盐酸环丙沙星、土霉素、恩诺沙星、硫酸新霉素、氨苄西林钠共9种药物的耐药性,同时用PCR法检测了该菌β-内酰胺酶基因bla CTX-M,喹诺酮类耐药基因(qnrVC,qnrVC5),四环素耐药基因(tetS、tetM)等耐药基因的携带情况。结果表明该菌对氨苄西林钠等药物耐药。对氟苯尼考、磺胺甲噁唑高度敏感。同时该菌携带bla CTX-M,qnrVC 2种耐药基因。本研究的结果为溶藻弧菌病的精准用药提供了数据支持。     

氨氮胁迫对凡纳滨对虾肠道免疫相关指标的影响

为研究急性氨氮胁迫对凡纳滨对虾(Litopenaeus vannamei)肠道免疫功能的影响,将对虾暴露于氨氮浓度为20 mg·L^-1的海水中72 h,测定了不同时间点肠道中抗病原感染指标如酸性磷酸酶(ACP)、碱性磷酸酶(ALP)、溶菌酶(Lys)、酚氧化酶原(proPO)以及抗氧化功能指标如总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、热休克蛋白70(HSP70)、热休克蛋白90(HSP90)等变化。结果显示,与对照组相比,氨氮胁迫后:1)ACP和ALP活性均于6 h显著升高(P<0.05),随后于48~72 h显著低于对照组(P<0.05);Lys活性于24 h显著升高至最大值(P<0.05),随后于72 h显著低于对照组(P<0.05)。2)T-AOC和SOD活性均于6 h和12 h显著高于对照组(P<0.05),随后于48 h和72 h显著降低(P<0.05)。3)HSP70基因表达水平于24 h显著升高至最大值,随后虽有降低,但仍显著高于对照组(P<0.05);HSP90和proPO基因表达水平均于12 h显著升高至最大值(P<0.05),随后于72 h降低至对照组水平(P>0.05)。研究表明,急性氨氮胁迫对凡纳滨对虾肠道免疫功能相关指标影响显著,对其肠道免疫防御系统有明显的损伤作用。     

益生菌与动物肠道自由基的关系

动物肠道益生菌具有免疫调节、形成肠黏膜上皮屏障功能和刺激肠道细胞增殖等多种生理作用。最新研究表明,益生菌一个重要作用机制是可通过调控肠道自由基的水平,既可发挥免疫调节作用,又避免了对肠道产生氧化损伤。益生菌能够刺激肠道细胞产生活性氧自由基(ROS),ROS参与调控肠道细胞内的氧化还原反应过程。同时,益生菌也能够利用其体内相关的酶系,清除肠道细胞产生的过量ROS,从而防止其对肠道的损伤作用。本文对益生菌通过调控肠道自由基水平,既可发挥免疫调节作用,又防止对肠道氧化损伤的功能及其相关机制进行了综述。     

免疫增强剂党参对仿刺参肠道菌群结构的影响

采用平板计数法和聚合酶链式反应( PCR)-变性梯度凝胶电泳( DGGE)技术分析免疫增强剂党参对仿刺参( Apostichopus japonicas)肠道菌群结构的影响。将初始体重为(18.00±2.00) g的仿刺参随机分为2组(对照组、试验组),每组6个重复,每个重复12只。对照组投喂海泥、鼠尾藻粉按照1∶1的质量比配制的饵料,试验组饵料中以鼠尾藻粉质量的2%添加党参,连续投喂28 d。结果表明：应用免疫增强剂党参不仅能够显著提高仿刺参的特定生长率( P<0.05),降低其饵料系数(P<0.05),而且能够显著增加仿刺参肠道内容物中异养菌的数量(P<0.05);序列统计分析显示投喂党参后仿刺参肠道细菌优质序列比例显著增加( P<0.05),试验组达97.57%,对照组仅为80.22%;Beta多样性分析反映投喂党参后仿刺参肠道微生态环境发生了变化,其多样性系数范围在14.91%~15.47%、15.47%~16.21%、14.91%~16.21%;丰度分析显示投喂党参后仿刺参肠道内容物中变形菌门( Proteobacteria)和拟杆菌门( Bacteroidetes)丰度提高,疣微菌门( Verrucomicrobia)、放线菌门( Actinobacteria)和厚壁菌门( Firmiaites)丰度降低;聚类分析显示试验组与对照组肠道菌群结构相似性系数为0.97。由此可见,免疫增强剂党参可提高仿刺参的特定生长率,降低饵料系数,增加肠道异养菌数量和优势菌群丰度,优化肠道微生态环境。     

外源精胺对断奶仔猪小肠黏膜成纤维细胞因子-2蛋白质表达量及小肠发育的影响

本试验旨在研究外源精胺对断奶仔猪小肠黏膜成纤维细胞因子-2( FGF2)蛋白质表达量及小肠发育的影响。将9窝胎次和初生体重相近的7日龄“杜×长×大”哺乳仔猪随机分配到0、12和15 mg/kg外源精胺组,每组3窝。仔猪从7日龄起补饲相应的饲粮,21日龄断奶后继续补饲断奶前饲粮至28日龄结束。从每窝选2头接近平均体重的仔猪屠宰,采集小肠及黏膜样品,测定FGF2蛋白质表达量和小肠的发育状况。结果表明：1)12 mg/kg外源精胺组仔猪小肠黏膜FGF2蛋白质表达量分别高于0和15 mg/kg外源精胺组,但3个外源精胺组仔猪小肠黏膜FGF2蛋白质表达量之间无显著差异(P>0.05)。2)12和15 mg/kg外源精胺组仔猪小肠绒毛高度和宽度分别极显著大于0 mg/kg外源精胺组( P<0.01),而12 mg/kg外源精胺组仔猪十二指肠和空肠黏膜绒毛高度与隐窝深度比值( V/C )分别极显著高于0 mg/kg外源精胺组( P<0.01)。3)28日龄仔猪小肠黏膜蔗糖酶和麦芽糖酶活性随外源精胺添加量的增加而升高。由此可见,给7~28日龄仔猪连续补饲外源精胺能提高28日龄仔猪小肠黏膜FGF2蛋白质表达量、V/C和二糖酶活性。     

Adenosine protects Sprague Dawley rats from high‐fat diet and repeated acute restraint stress‐induced intestinal inflammation and altered expression of nutrient transporters

This study investigated the effect of repeated acute restraint stress and high‐fat diet (HFD) on intestinal expression of nutrient transporters, concomitant to intestinal inflammation. The ability of adenosine to reverse any change was examined. Six‐week‐old male Sprague Dawley rats were divided into eight groups: control or non‐stressed (C), rats exposed to restraint stress for 6 h per day for 14 days (S), control rats fed with HFD (CHF) and restraint‐stressed rats fed with HFD (SHF); four additional groups received the same treatments and were also given 50 mg/l adenosine dissolved in drinking water. Fasting blood glucose, plasma insulin, adiponectin and corticosterone were measured. Intestinal expression of SLC5A1, SLC2A2, NPC1L1 and TNF‐α was analysed. Histological evaluation was conducted to observe for morphological and anatomical changes in the intestinal tissues. Results showed that HFD feeding increased glucose and insulin levels, and repeated acute restraint stress raised the corticosterone level by 22%. Exposure to both stress and HFD caused a further increase in corticosterone to 41%, while decreasing plasma adiponectin level. Restraint stress altered intestinal expression of SLC5A1, SLC2A2 and NPC1L1. These changes were enhanced in SHF rats. Adenosine was found to alleviate HFD‐induced increase in glucose and insulin levels, suppress elevation of corticosterone in S rats and improve the altered nutrient transporters expression profiles. It also prevented upregulation of TNF‐α in the intestine of SHF rats. In summary, a combination of stress and HFD exaggerated stress‐ and HFD‐induced pathophysiological changes in the intestine, and biochemical parameters related to obesity. Adenosine attenuated the elevation of corticosterone and altered expression of SLC5A1, NPC1L1 and TNF‐α.