中链甘油三酯对脂多糖刺激小鼠血液指标与肝脏抗氧化功能的影响

试验旨在研究中链甘油三酯(MCT)对脂多糖(LPS)刺激小鼠血液指标与肝脏抗氧化功能的影响。将40只昆明小鼠用2×2试验因子设计分成4组,主因子包括:日粮(10%豆油或"8%MCT+2%豆油")和免疫应激(注射LPS或生理盐水)。试验第28天,每个日粮组的5只小鼠注射150μg/kg体重的LPS,另5只注射无菌生理盐水作为对照。结果表明:与对照组相比,LPS显著降低了小鼠血浆葡萄糖、总蛋白水平及肝脏总抗氧化能力(P0.05),LPS刺激后小鼠血浆白介素-1β含量呈升高趋势(P=0.051);与长链甘油三酯(LCT)相比,MCT显著提高了血浆总蛋白、白蛋白含量(P0.05),并降低了总胆固醇水平(P0.05);MCT组血浆总甘油三酯(P=0.055)水平与肝脏总抗氧化能力(P=0.081)较LCT组呈升高趋势,肝脏丙二醛含量相对较低(P=0.091)。MCT降低了LPS刺激后小鼠机体葡萄糖的消耗,改善蛋白质代谢与肝脏抗氧化能力。     

咖啡因对小鼠免疫功能和抗氧化能力的影响

通过检测不同组别小鼠胸腺指数、脾脏指数、SOD含量以及MDA含量的变化,探究不同剂量的咖啡因对小鼠免疫功能和抗氧化能力的影响.结果表明:高剂量咖啡因(20mg/kg)可显著抑制小鼠免疫功能并降低其抗氧化能力.本实验为研究咖啡因对机体影响提供一定科学依据.     

N-乙酰半胱氨酸对脂多糖刺激仔猪空肠黏膜抗氧化能力的影响

本试验旨在研究N-乙酰半胱氨酸(NAC)对脂多糖(LPS)慢性刺激仔猪空肠黏膜抗氧化能力的影响.选用18头健康仔猪[平均体重为(11.58±0.26)kg],随机分为3个组(对照组、LPS组、NAC组),每组6个重复,每个重复1头猪.对照组和LPS组饲喂基础饲粮,NAC组饲喂基础饲粮+0.05%NAC.在试验第10天、...     

桦木酸对小鼠免疫器官抗氧化能力的影响

本试验旨在研究桦木酸(BA)对小鼠免疫器官抗氧化能力的影响.选取健康的昆明系小鼠28只,随机分为4组(每组7只),每天每只分别按每千克体重0、0.25、0.50、1.00 mg的剂量给予BA,BA混悬于0.2 mL1％可溶性淀粉溶液中.以灌胃方式给予,每天灌胃1次,连续灌胃14 d后,检测各组小鼠脾脏和胸腺中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GHS-Px)活性,丙二醛(MDA)含量以及总抗氧化能力(T-AOC).结果表明:BA可使小鼠脾脏和胸腺中SOD、GSH-Px活性以及T-AOC升高,MDA含量降低.其中,每千克体重灌胃0.50 mg BA能显著或极显著提高脾脏和胸腺中GSH-Px活性和T-AOC(P＜0.05或P＜0.01),显著或极显著降低胸腺和脾脏中MDA含量(P＜0.05或P＜0.01);每千克体重灌胃1.00 mg BA能显著或极显著提高脾脏和胸腺中SOD活性、T-AOC以及脾脏中GSH-Px活性(P＜0.05或P＜0.01),极显著降低胸腺和脾脏中MDA含量(P＜0.01).由此得出,BA能有效地增强小鼠免疫器官的抗氧化能力.     

苹果原花青素对小鼠运动能力和抗氧化能力的影响

为研究苹果中原花青素对小鼠运动能力和抗氧化能力的影响,选取5周龄健康雄性小鼠45只,随机分为3组,进行3周适应性游泳训练。小鼠运动结束后,通过轻度麻醉条件下采集血液和肌组织,检测血清中乳酸(LD)和丙二醛(MDA)含量,以及测定超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活力。结果表明,各组小鼠的初始体重对比无显著差异(P0.05);运动对照组和试验组小鼠的游泳至力竭的时间明显长于安静对照组;与运动对照组相比,试验组小鼠的游泳至力竭的时间也呈现明显的延长趋势(P0.05)。游泳运动以后,运动对照组和试验组小鼠血清和肌组织中LD和MDA含量明显低于安静对照组;与运动对照组相比,试验组小鼠的血清LD和MDA含量也呈现明显下降趋势(P0.05)。另外,运动对照组和试验组小鼠SOD和CAT活性明显高于安静对照组,且与运动对照组相比,试验组SOD和CAT活性显著升高(P0.05)。说明苹果原花青素能提高小鼠运动能力和抗氧化能力,且与有氧运动相结合能够产生协同效应,具有较好的应用前景。     

阿魏酸对脂多糖应激的吉林白鹅生长性能和肠道抗氧化指标的影响

【目的】研究阿魏酸(FA)对脂多糖(LPS)诱导的氧化应激吉林白鹅生长性能、脏器系数以及肠道抗氧化指标的影响,为FA在鹅养殖过程中缓解氧化应激提供参考。【方法】选取7日龄健康雄性吉林白鹅120只,并随机分成6组(每组5个重复,每个重复4只):K组(空白对照组,基础饲粮)、L组(LPS对照组,基础饲粮)和A、B、C、D组(基础饲粮中分别添加60、120、180和240 mg/kg FA),在正式试验第14、17、20天时,L、A、B、C和D组腹腔注射0.5 mg/kg LPS,K组注射等体积的生理盐水,第21天时每组随机选取10只进行屠宰,取心脏、肝脏、脾脏、肾脏、法氏囊、胸腺,称重并计算脏器系数;分离十二指肠、空肠和回肠,用于测定肠道抗氧化指标。【结果】(1)第1～14天,与L组相比,C组的终末体重(FB)、平均日采食量(ADFI)、平均日增重(ADG)显著升高,而料重比(F/G)显著下降(P<0.05),且除ADFI显著高于K组外,其他指标均与K组差异不显著(P>0.05);第15～21天,与L组相比,A、B、C和D组FB、ADG、ADFI显著升高,F/G显著降低(P&l...     

脂多糖对体外培养奶牛子宫内膜上皮细胞子宫容受性因子表达的影响

试验旨在通过脂多糖（lipopolysaccharide,LPS）诱导奶牛子宫内膜上皮细胞构建子宫内膜炎体外感染模型,研究子宫内膜炎对奶牛子宫容受性因子大分子转膜黏蛋白-糖蛋白1（MUC-1）、高度保守的分泌型WNT家族亚型糖蛋白（Wnt-7a）、β受体1（IFNAR1）、IFNAR2、Integrin αvβ3 mRNA及蛋白相对表达量的影响,进而阐明子宫内膜炎引起奶牛屡配不孕和繁殖率低下的机制。采用组织块法分离培养奶牛子宫内膜上皮细胞,免疫荧光方法鉴定细胞纯度,不同浓度LPS刺激子宫内膜上皮细胞,在不同时间点用CCK8测定细胞存活率,ELISA检测炎性因子白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）、IL-6、IL-8的分泌变化,实时荧光定量PCR和Western blotting分别检测子宫内膜感染模型中子宫容受性因子MUC-1、Wnt-7a、IFNAR1、IFNAR2、Integrin αvβ3 mRNA及蛋白的表达变化。结果显示,通过组织块法纯化获得的奶牛子宫上皮细胞数量较多,经免疫荧光角蛋白染色证实纯度较高。采用CCK8测定细胞存活率发现,与对照组相比,浓度为0、5、10、50μg/mL的LPS作用6、12、24、48 h后,细胞活力无显著变化（P>0.05）;浓度为100μg/mL的LPS作用24 h时,细胞存活率显著低于对照组（P<0.05）,细胞培养上清中的IL-1β、TNF-α、IL-6、IL-8含量均显著高于对照组及低浓度组（P<0.05）,引起细胞的炎症反应。与对照组相比,模型组MUC-1 mRNA及蛋白的相对表达量均极显著增加（P<0.01）;Wnt-7a mRNA及蛋白的相对表达量均极显著下降（P<0.01）;Integrin αvβ3、IFNAR1和IFNAR2 mRNA相对表达量均极显著下降（P<0.01）,蛋白相对表达量均显著下降（P<0.05）。结果表明,浓度为100μg/mL的LPS作用24 h可成功构建子宫内膜炎体外感染模型,子宫内膜炎对奶牛子宫容受性因子MUC-1、Wnt-7a、IFNAR1、IFNAR2、Integrin αvβ3 mRNA及蛋白表达的影响可能是引起奶牛屡配不孕和繁殖率低下的重要原因。     

谷氨酰胺对脂多糖诱导的断奶仔猪氧化应激的影响

本试验以大肠杆菌型脂多糖(LPS)建立氧化应激模型,探讨了谷氨酰胺(GLN)对断奶仔猪氧化应激的影响。选用24头28日龄的健康三元(杜×长×大)断奶仔猪,随机分成3组,每组8个重复,每个重复1头猪。对照组和应激组饲喂基础饲粮,GLN组饲粮在基础饲粮中添加1%GLN,试验期为30 d。在试验第22、25、28和30天,应激组和GLN组仔猪分别按每千克体重腹腔注射100μg LPS,对照组仔猪腹腔注射相同剂量的灭菌生理盐水,第30天进行前腔静脉采血并屠宰采取所需肠道样品,检测氧化应激相关指标。结果显示:1)LPS攻毒前各组血清抗氧化能力指标均无显著差异(P0.05)。LPS攻毒后,应激组血清丙二醛(MDA)含量显著高于对照组(P0.05);GLN组血清MDA含量和超氧化物歧化酶(SOD)活性显著低于应激组和对照组(P0.05)。2)LPS攻毒后,在十二指肠黏膜中,GLN组过氧化氢酶(CAT)和锌铜超氧化物歧化酶(Cu Zu SOD)基因相对表达量显著高于应激组(P0.05)。在空肠黏膜中,GLN组CAT、锰超氧化物歧化酶(Mn SOD)、谷胱甘肽过氧化物酶1(GPX1)和谷胱甘肽过氧化物酶4(GPX4)基因相对表达量显著高于对照组和应激组(P0.05),对照组GPX4基因相对表达量显著高于应激组(P0.05)。在回肠黏膜中,GLN组和应激组CAT基因相对表达量显著低于对照组(P0.05),GPX4基因相对表达量显著高于对照组(P0.05);GLN组Mn SOD基因相对表达量显著高于对照组和应激组(P0.05),Cu Zn SOD基因相对表达量显著高于对照组(P0.05)。结果表明,GLN在一定程度上可以缓解断奶仔猪因LPS引起的氧化应激,以期为实际生产中减少氧化应激提供一定的理论基础。     

母牛产后子宫隐性感染对子宫复旧的影响

母牛产后子宫隐性感染对子宫复旧的影响刘崇立王运亨周玉云（北京西郊农场，１０００９４）李强卢长泉（北京市北郊农场）于德洪（北京奶牛中心）母牛生殖道狭窄或因胎儿过大，易造成难产。难产时由于产道过度扩张、胎产滞留时间较长等，容易引起母牛产后子宫的感染。造成...     

Effect of intramammary infusion of bacterial lipopolysaccharide on experimentally induced Staphylococcus aureus intramammary infection

Mastitis due to Staphylococcus aureus is a significant problem in the dairy industry and is refractory to antibiotic treatment and/or vaccine prevention. Relative to other mastitis-causing pathogens, S. aureus elicits a diminutive host inflammatory response during intramammary infection. To determine whether induction of a heightened inflammatory response could influence outcome of infection, the highly pro-inflammatory molecule bacterial lipopolysaccharide (LPS) was infused into udder quarters experimentally infected with S. aureus. Relative to S. aureus-infected udder quarters receiving saline, quarters infused with LPS demonstrated a heightened inflammatory response as demonstrated by the induction of TNF-alpha and higher milk somatic cell counts and albumin levels. Although there was no overall effect on bacterial clearance, a trend toward reduced bacterial numbers during the immediate pro-inflammatory response following LPS infusion was observed suggesting that this novel approach to treating S. aureus intramammary infection may warrant further investigation.     

猪布鲁菌感染对巨噬细胞泛素蛋白酶体功能的影响

巨噬细胞(macrophage,M_φ)是布鲁菌的主要宿主细胞,为了探明布鲁菌感染与M_φ泛素-蛋白酶体功能之间的关系,本试验在应用蛋白酶体抑制剂Lactacystin与促进剂IFN-γ的基础上,对M_φ感染猪种布鲁菌S2株(Brucella suis,B.suis)后细胞上清中泛素、蛋白酶体及胞内B.suis数量进行了检测。结果显示,IFN-γ与Lactacystin对M_φ泛素的表达均有明显的促进作用,且IFN-γ效果显著优于Lactacystin;其次IFN-γ有效促进了M_φ蛋白酶体的表达,而Lactacystin显著抑制了M_φ蛋白酶体的表达。在此基础上,将B.suis感染不同状态的M_φ,在0.5~24h分别进行胞内B.suis计数,研究表明,一方面B.suis的感染促进了M_φ泛素及蛋白酶体的表达;另一方面,泛素蛋白酶体系统功能的增强,显著降低了B.suis的早期感染,但对于B.suis感染中后期作用不明显,而感染后期抑制M_φ蛋白酶体功能,却可显著降低B.suis的胞内增殖能力。     

Involvement of the fas ligand and fas system in apoptosis induction of mouse uterine natural killer cells

Uterine natural killer (uNK) cells in the pregnant uterus are known to be associated with the normal development of the placenta. In the mouse pregnant uterus, many uNK cells exist during mid pregnancy, although they show a sudden decrease during late pregnancy and almost disappear before delivery. Our previous study indicated that uNK cells showed clear apoptotic morphology during late pregnancy. Therefore, the present study was carried out to define the involvement of Fas ligand (FasL) and Fas in apoptosis induction of uNK cells. Immunohistochemical analyses revealed that uNK cells expressed FasL in the cytoplasmic granules and Fas on the cell membrane during late pregnancy. In lpr/lpr mice, which genetically lack Fas, many uNK cells were clearly observed during late pregnancy compared with wild-type mice, and moreover uNK cells still existed at day-18 of pregnancy, although there were few in wild-type mice during the same period. In the experiment of in vitro culture, uNK cells derived from wild-type placenta showed chromatin condensation and DNA fragmentation frequently following the anti-Fas antibody treatment, as compared with the control. From these results, it is suggested that FasL and Fas-dependent apoptosis regulates cell appearance of uNK cells in the mouse pregnant uterus.     

Plasma lipopolysaccharide elevations in cattle associated with early-stage infection by Fasciola hepatica

Fasciolosis is an endemic zoonotic parasitic disease with significant impacts on human health and both animal health and production. Early post-infection impacts on the host remain unclear. The objective of this study was to determine the changes, if any, to levels of endotoxin in cattle plasma in response to early-stage infection with Fasciola hepatica. Thirty-six (36) commercial bred cattle were experimentally infected with approximately 400 viable metacercariae. Plasma lipopolysaccharide (endotoxin) levels were examined on 24 occasions from 0 h before infection to 336 h after infection using the Limulus Amoebocyte Lysate chromogenic end point assay and compared with that of six (6) uninfected control animals. Peak lipopolysaccharide levels in infected animals were reached at 52 h after infection and returned to pre-infection levels at time 144 h after infection. Infected animals had significantly elevated lipopolysaccharide levels between 24 and 120 h after infection when compared to uninfected animals. The mean change in endotoxin units (EU)/mL over time after infection was statistically significant in infected animals. Elevations of lipopolysaccharide occurred in all infected animals suggesting a possible repeatable and titratable endotoxemia conducive to therapeutic agent model development.     

奶牛产后子宫内细菌内毒素与子宫内膜炎的关系

试验通过对15头经严怀孕奶牛,严后1～9d提取严后子宫内容物样品,进行子宫内细菌内毒素的测定,探讨产后子宫内细菌内毒素与产后子宫内膜炎的关系。结果显示,产后第3～9天,子宫内细菌内毒素升高极显著（P〈0．01）的奶牛,经后来的调查发现发生子宫内膜炎。初步认为通过早期检测产后子宫内细菌内毒素的方法为预测子宫是否发生感染提供一定的依据。     

Effect of Nigella sativa on glucose concentration, lipid peroxidation, anti-oxidant defence system and liver damage in experimentally-induced diabetic rabbits

This study was carried out to investigate whether Nigella sativa could decrease the lipid peroxidation, increase the anti-oxidant defence system and also prevent the lipid-peroxidation-induced liver damage in experimentally induced diabetic rabbits. Fifteen New Zealand male rabbits were divided into three experimental groups: control, diabetic and diabetic and N. sativa-treated. The diabetes mellitus (DMI) was induced in the rabbits using 150 mg/kg of 10% alloxan. The diabetic + N. sativa-treated group was given extract of N. sativa seeds orally every day for 2 months after induction of DM. At the end of the 2-month experiment, blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), ceruloplasmin and glucose concentration, and livers were harvested for histopathological analysis. Treatment with N. sativa decreased the elevated glucose and MDA concentrations, increased the lowered GSH and ceruloplasmin concentrations, and prevented lipid-peroxidation-induced liver damage in diabetic rabbits. It was concluded that N. sativa might be used in diabetic patients to prevent lipid peroxidation, increase anti-oxidant defence system activity and also prevent liver damage.     

Experimental infection of the white-footed mouse with Borrelia burgdorferi

Laboratory raised white-footed mice (Peromyscus leucopus) were inoculated experimentally with live spirochetes (Borrelia burgdorferi), the etiologic agent of Lyme disease (borreliosis). Prior to inoculation, mouse sera were tested with an indirect fluorescent antibody test, and all mice were seronegative. All inoculated mice seroconverted. In tick transmission studies, immature stages of Ixodes dammini and Dermacentor variabilis attached and fed to repletion on mice, but only I dammini transferred spirochetes to uninfected mice. Mice were susceptible to oral infection and transmitted infection to each other through direct contact. Infection did not affect reproduction or development of young born from infected dams, nor did spirochetes appear in the tissues of neonates. Borrelia burgdorferi spirochetes were identified in the kidneys, liver, and spleen of infected mice by the use of the modified Steiner silver stain and a tissue indirect fluorescent antibody test. Spirochetes also were isolated in culture of the heart blood of 1 mouse. Regardless of the source of infection, no mice developed clinical signs or had any pathologic change resulting from infection. Spirochetes were always observed extracellularly within interstitial spaces. Antibody titers persisted for over 4 months in some mice and spirochetes were found in the tissues of 1 mouse that had been infected 1 year earlier.     

Effects of antimicrobial peptides derived from the beetle Allomyrina dichotoma defensin on mouse peritoneal macrophages stimulated with lipopolysaccharide

We previously reported that synthetic peptides, RLYLRIGRR-NH2 (peptide A) and RLRLRIGRR-NH2 (peptide B), derived from the beetle Allomyrina dichotoma defensin, showed antimicrobial activity against both Gram-positive and negative bacteria and suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) mRNA expression in a murine macrophage cell line. In this study, inhibitory effects of these peptides in LPS-induced mouse peritoneal macrophage activation were investigated. The supplement of peptide A to macrophages cultured with LPS resulted in a significant decrease in nitric oxide and TNF-alpha production. Furthermore, NF-kappaB activation was also blocked by addition of peptide A. These results indicated that peptide A blocked macrophage activation induced by LPS.