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1.
利用手术结合化学造模法,建立血栓闭塞性脉管炎大鼠模型,并运用病理学、免疫学及分子生物学方法对模型进行鉴定。结果显示,利用股动脉注射月桂酸钠的方法,成功构建类似于人血栓闭塞性脉管炎的大鼠动物模型。模型大鼠病变明显,病变部位血管内皮细胞Icam-1、Vcam-1 mRNA表达显著升高,模型大鼠血清中TXB2、AECA含量显著升高,与人血栓闭塞性脉管炎自然发病病理特点相似。本试验构建的血栓闭塞性脉管炎大鼠模型可用于进一步研究,可为该疾病发病机理研究与治疗方法探索提供平台。 相似文献
2.
目的：探讨蕨麻多糖（PAP）对小鼠脾淋巴细胞内花生四烯酸（AA）代谢产物的影响。方法：用放射免疫方法检测了血栓素B2（TXB2）和6-酮-前列腺素F1α（6-K-PGF1α）在细胞内的含量。结果：不同蕨麻多糖浓度组，6—K—PGF1α含量达到高峰的时间段各不相同；与对照组相比较，100μg／ml PAP组TXB2的含量明显偏低，而其它各组在同一时间段TXB2含量与多糖浓度呈剂量依赖关系；并且PGF1α／TXB2比值也随PAP浓度递增而升高。结论：PAP能调节小鼠脾淋巴细胞AA代谢水平和机体PGF1α／TXB2平衡状态，影响机体免疲机能。 相似文献
3.
【目的】 探究芒果苷（mangiferin，Man）对鸭甲型肝炎病毒1型（Duck hepatitis A virus-1，DHAV-1）致鸭胚肝细胞（DEHCs）炎性损伤的影响。【方法】 从14日龄SPF级麻鸭鸭胚肝脏组织分离原代DEHCs，用含不同浓度芒果苷（0、5、10、20、40、80和160 μmol/L）的培养液培养48 h后，通过CCK-8法检测其安全浓度范围；用安全浓度的芒果苷培养DEHCs 12、24和48 h后，检测培养液上清中乳酸脱氢酶（LDH）的活力，判定芒果苷对DEHCs的毒性作用。将DEHCs分为对照组（Mock）、模型组（Model）、芒果苷组（Man10、Man20和Man40）和利巴韦林组（Rib），每组3个重复，所有组细胞血清饥饿培养12 h后，Mock组加入含10%胎牛血清（FBS）的DMEM培养基，Model、Man10、Man20、Man40和Rib组用DHAV-1（MOI=1.0）攻毒2 h后，Model组更换为含10% FBS的DMEM培养基，Man10、Man20、Man40培养基中分别添加10、20和40 μmol/L芒果苷，Rib组添加1 μmol/L利巴韦林。48 h后收集各组细胞，用比色法检测丙二醛（MDA）含量及过氧化氢酶（CAT）、总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、总一氧化氮合酶（T-NOS）和谷胱甘肽过氧化物酶（GSH-Px）的活性；免疫荧光（IF）法检测DHAV-1在各组DEHCs中的分布情况；Western blotting法检测NLRP3/Pro-Caspase1/IL-1β通路蛋白的表达情况。提取2日龄SPF麻鸭的新鲜全血，分离鸭外周血单个核细胞（duPBMCs），duPBMCs分组及处理同DEHCs，ELISA法检测各组duPBMCs上清液中白介素8（IL-8）和IL-1β的含量。【结果】 与0 μmol/L芒果苷组相比，80和160 μmol/L芒果苷组细胞的增殖能力显著降低（P<0.05），因此5~40 μmol/L芒果苷为处理DEHCs的安全给药浓度。20和40 μmol/L芒果苷处理48 h细胞上清液中LDH活力显著低于处理12和24 h （P<0.05），20和40 μmol/L芒果苷处理12和24 h细胞上清液中LDH活力显著高于5和10 μmol/L芒果苷处理（P<0.05），各浓度芒果苷处理48 h细胞上清液中LDH活力均差异不显著（P>0.05），故48 h为最适处理时间。与Mock组相比，Model组DEHCs中CAT、T-AOC、SOD和GSH-Px活性均显著降低（P<0.05），DEHCs中MDA含量、T-NOS活性、DHAV-1拷贝数、DHAV-1阳性率、NLRP3表达量及duPBMCs中IL-8、IL-1β分泌量均显著升高（P<0.05）。与Model组相比，Man10、Man20和Man40组DEHCs中CAT、T-AOC、SOD和GSH-Px活性均显著提高（P<0.05），DEHCs中MDA含量、T-NOS活性、DHAV-1拷贝数、DHAV-1阳性率、NLRP3表达量及duPBMCs中IL-8、IL-1β分泌量均显著降低（P<0.05）。【结论】 芒果苷可通过增加抗氧化能力、降低DHAV-1的复制水平、抑制NLRP3通路的激活、降低促炎细胞因子的释放抗DHAV-1感染DEHCs造成的炎性损伤。 相似文献
4.
试验旨在通过改良彗星实验检测黄曲霉毒素B1（aflatoxin-B1,AFB1）对雏鸭肝细胞DNA损伤的影响。雏鸭经AFB1灌胃染毒,2 h后分离肝细胞,并通过改良彗星实验测定DNA损伤。结果显示,AFB1能够导致雏鸭肝细胞DNA损伤,表现为〖JP2〗尾长、尾部DNA百分含量、尾矩、Olive尾矩等彗星参数与空白和溶剂对照组相比显著增加（P<0.05）。表明改良彗星实验能够用于AFB1导致肝细胞DNA损伤的检测,试验还提示,在体肝细胞彗星实验能够作为雏鸭AFB1暴露的遗传毒性标志物。 相似文献
5.
用结扎颈动脉和缺氧的方法建立一侧缺氧缺血性脑损伤(HIE)动物模型,观察脑活素对HIE大鼠脑组织损伤的治疗作用。结果发现,缺氧缺血后新生大鼠脑组织血栓素B2(TXB2)和6酮--前列腺素F1α(6-keto-PGF1α)含量、细胞凋亡数及对侧脑组织含水量均显著升高,表明新生大鼠缺氧缺血性脑损伤与脑血流改变、脑细胞凋亡及脑组织含水量的变化密切相关;缺氧缺血大鼠应用脑活素治疗后,其脑组织TXB2和6-keto-PGF1α含量、细胞凋亡数及脑组织含水量均下降,表明脑活素通过改善脑血流、降低脑细胞凋亡及脑水肿程度来减轻缺氧缺血造成的损伤,对新生大鼠缺氧缺血性脑损伤发挥有效的治疗作用。 相似文献
6.
以正常人肝细胞（L-02细胞）为研究对象,根据细胞增殖率、活性氧（reactive oxygen species,ROS）含量、丙二醛（malondialdehyde,MDA）含量等指标的变化研究黄曲霉毒素B1（aflatoxin B1,AFB1）的毒性作用及氧化应激损伤,选用VC作为AFB1损伤肝细胞的保护剂,通过比色法测定细胞的相对存活率,从细胞周期的变化和细胞凋亡率研究AFB1引起L-02细胞凋亡的程度及机制。结果表明：根据AFB1的半数细胞抑制率（inhibition of cell,IC）（IC 相似文献
7.
试验旨在研究抗菌肽Temprine-La（S）（T-La（S））、Temprine-La（FS）（T-La（FS））、RGD-T-La（S）和RGD-T-La（FS）对2型猪链球菌（SS2）生物被膜形成的抑制作用。通过结晶紫染色法（CV）检测SS2生物被膜形成能力；微量稀释法测定抗菌肽对SS2生物被膜的最小生物被膜抑菌浓度（MBIC）和最小生物被膜杀菌浓度（MBEC）；结晶紫染色法和扫描电镜（SEM）检测抗菌肽对SS2生物被膜形成的影响；XTT法检测抗菌肽对SS2生物被膜代谢活性的影响；苯酚硫酸法检测抗菌肽对SS2生物被膜胞外多糖含量的影响；建立猪链球菌-斑马鱼感染模型，HE染色法观察T-La（FS）对斑马鱼脑组织病理变化的影响；实时荧光定量PCR法分析抗菌肽对SS2生物被膜相关基因及对斑马鱼炎性细胞因子基因转录水平的影响。结果显示，SS2具有良好的生物被膜形成能力；T-La（S）、RGD-T-La（S）、T-La（FS）和RGD-T-La（FS）对SS2生物被膜的MBIC分别为31.3、15.6、7.8和15.6 μg/mL；MBEC分别为62.6、31.2、15.6和31.2 μg/mL；结晶紫染色结果表明，抗菌肽对SS2生物被膜的形成有抑制作用；扫描电镜结果显示，抗菌肽使SS2生物被膜中的细菌数量和生物被膜的形态发生明显变化，细胞外基质大量减少；XTT法结果显示，抗菌肽可显著降低SS2生物被膜的代谢活性；苯酚硫酸法结果显示，抗菌肽能有效抑制SS2生物被膜合成胞外多糖；实时荧光定量PCR结果表明，抗菌肽作用后降低了SS2生物被膜基因的转录水平；T-La（FS）作用后TLR2、MyD88及促炎性细胞因子基因的转录水平显著或极显著降低（P<0.05；P<0.01），抗炎性细胞因子基因的转录水平显著或极显著升高（P<0.05；P<0.01）。抗菌肽主要通过影响生物被膜相关基因转录水平和阻断胞外多糖的合成与分泌来抑制SS2生物被膜的形成，其中T-La（FS）可能通过抑制TLR2信号通路中TLR2和MyD88分子表达，抑制炎性细胞因子的释放，减轻脑膜炎的炎性反应。 相似文献
8.
为研究microRNA-124-3p（miR-124-3p）对H1N1亚型猪流感病毒（swine influenza virus，SIV）感染小鼠所致肺损伤的调控作用，本试验构建miR-124-3p腺病毒表达载体，通过小鼠尾部静脉注射法构建miR-124-3p差异表达小鼠模型，试验分3组：过表达组、抑制组和对照组。48 h后，各组小鼠鼻腔接种H1N1亚型SIV，每只105 EID50（50 μL）。连续观察14 d，计算小鼠平均体重变化率、观察病理切片并测定相关炎症因子IL-1β、TNF-α和IL-6 mRNA相对表达量。结果显示，已成功将pre-miR序列及其sponge序列插入腺病毒的穿梭质粒，并将其共转染293A细胞。实时荧光定量PCR检测证实，与对照组相比，过表达组和抑制组小鼠黑色素瘤细胞miR-124-3p表达水平分别极显著升高（P<0.01）和显著降低（P<0.05），表明成功构建腺病毒表达载体。过表达组、抑制组和对照组小鼠体重变化率分别为－5.5%、－12.4%和－8.6%。抑制组和对照组均可见肺泡壁增厚，其间有多量淋巴细胞浸润，部分肺泡内出现纤维蛋白渗出，且抑制组病理变化更为严重，肺泡中还有大量的红细胞浸润；而过表达组仅有少量的淋巴细胞浸润，肺脏组织较正常。与对照组相比，过表达组检测的炎症因子IL-1β、TNF-α和IL-6 mRNA表达水平均显著降低（P<0.05）；抑制组炎症相关炎症因子mRNA表达水平均显著升高（P<0.05）。本试验结果表明，miR-124-3p对H1N1亚型SIV感染小鼠所致的肺脏炎症因子的表达具有抑制作用，同时能减轻肺脏病理损伤。 相似文献
9.
以体外培养的仔猪睾丸支持细胞为研究对象，研究了FSH对GDNF蛋白的调节及其信号传导机制。结果显示：（1）外源性FSH以浓度和时间依赖性促进GDNF蛋白表达：FSH浓度为50ng／mL、作用1h时，GDNF水平达到最高；（2）用FSH（50ng／mL）或dbcAMP（100μmol／L）处理支持细胞，可迅速激活MEK激酶，随FSH刺激时间的延长，ERK1／2活性逐渐升高（0～2h）；（3）MEK1／2的抑制剂U0126可显著抑制FSH对GDNF的激活作用。结果表明，FSH在诱导GDNF蛋白表达的过程中，通过cAMP-PKA-ERK1／2级联通路，促进GDNF基因的表达。 相似文献
10.
1,25（OH）2D3是维生素D的主要活性形式,影响人和动物脂肪形成,为探究其在猪脂肪细胞增殖分化中的作用,试验从3~5日龄仔猪皮下脂肪组织分离培养前体脂肪细胞,并以浓度为0、0.1、1、10、100和1 000 nmol/L的1,25（OH）2D3分别处理,在培养的0、1、2、4、6、8和10 d采用MTT比色法检测细胞增殖活性;在诱导分化后0、1、2、4、6、8和10 d,以油红O染色提取法和实时荧光定量PCR检测细胞成脂分化及分化标志基因过氧化物酶体增殖物激活受体γ（PPARγ）和脂肪酸合成酶（FAS）表达。结果显示,0.1和1 nmol/L 1,25（OH）2D3显著促进猪前体脂肪细胞增殖（P<0.05）,而浓度为10~100 nmol/L时则抑制细胞增殖（P<0.05）;0.1和1 nmol/L 1,25（OH）2D3显著抑制猪前体脂肪细胞分化（P<0.05）,降低PPARγ和FAS mRNA表达水平（P<0.05）,但在浓度为10和100 nmol/L时,显著促进猪前体脂肪细胞分化（P<0.05）,上调PPARγ和FAS mRNA表达（P<0.05）;浓度达1 000 nmol/L时,可能对细胞有毒性作用。综合以上结果,低浓度1,25（OH）2D3促进猪前体脂肪细胞增殖,而通过下调PPARγ表达抑制分化;高浓度1,25（OH）2D3抑制猪前体脂肪细胞增殖,通过上调PPARγ表达促进分化。1,25（OH）2D3对猪前体脂肪细胞增殖和分化具有双向作用。 相似文献
11.
Cell adhesion molecules, leukocyte trafficking, and strategies to reduce leukocyte infiltration 总被引：6，自引：0，他引：6
Radi ZA Kehrli ME Ackermann MR 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2001,15(6):516-529
Leukocyte-endothelial cell interactions are mediated by various cell adhesion molecules. These interactions are important for leukocyte extravasation and trafficking in all domestic animal species. An initial slowing of leukocytes on the vascular endothelium is mediated by selectins. This event is followed by (1) activation of beta2 integrins after leukocyte exposure to cytokines and pro-inflammatory mediators, (2) adherence of leukocyte beta2 integrins to vascular endothelial ligands (eg, intercellular adhesion molecule-1 [ICAM-1]), (3) extravasation of leukocytes into tissues through tight junctions of endothelial cells mediated by platelet and endothelial cell adhesion molecule-1 (PECAM-1), and (4) perivascular migration through the extracellular matrix via beta1 integrins. Inhibiting excessive leukocyte egress and subsequent free radical-mediated damage caused by leukocyte components may attenuate or eliminate tissue damage. Several methods have been used to modify leukocyte infiltration in various animal models. These methods include nonspecific inhibition of pro-inflammatory mediators and adhesion molecules by nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, inhibition of cytokines and cytokine receptors, and inhibition of specific types of cell adhesion molecules, with inhibitors such as peptides and antibodies to beta2 integrins, and inhibitors of selectins, ICAMs, and vascular cell adhesion molecule-1 (VCAM-1). By understanding the cellular and molecular events in leukocyte-endothelial cell interactions, therapeutic strategies are being developed in several animal models and diseases in domestic animal species. Such therapies may have clinical benefit in the future to overcome tissue damage induced by excessive leukocyte infiltration. 相似文献
12.
本试验旨在研究黄芪多糖(Astragalus polysaccharin,APS)对肉鸡外周血淋巴细胞(peripheral lymphocyte,PLC)与颈静脉内皮细胞(jugular vein endothelial cells,JVEC)间黏附的影响。以4种剂量的APS (0、200、600和1000 μg/mL)分别处理肉鸡JVEC和PLC,观察二者间黏附量的变化;以白介素-1(IL-1,1000 U/mL)和肿瘤坏死因子-α(TNF-α,1000 U/mL)分别与4种剂量的APS(0、200、600和1000 μg/mL)共同处理JVEC和PLC,观察不同剂量APS对PLC与JVEC间黏附的影响,及对JVEC表面细胞间黏附分子-1(ICAM-1)和PLC表面CD4+变化的调节。结果表明,600 μg/mL APS处理JVEC,可显著增加PLC与JVEC间的黏附(P<0.05);IL-1与高剂量的APS(1000 μg/mL)共同处理JVEC或IL-1与3种剂量的APS(200、600和1000 μg/mL)共同处理PLC,均能显著增加PLC与JVEC间的黏附(P<0.05);与对照组相比,TNF-α单独处理JVEC后可显著增加PLC与JVEC间的黏附(P<0.05);与对照组相比,IL-1与高剂量APS (1000 μg/mL)共同处理JVEC后可显著增加JVEC表面ICAM-1值(P<0.05),IL-1与高剂量APS (1000 μg/mL)共同处理PLC后可显著增加PLC表面CD4+阳性细胞百分率(P<0.05)。综上所述,APS调控PLC与JVEC间黏附受其剂量的影响,在本试验条件下,中、高剂量APS(600和1000 μg/mL)单独或与IL-1、TNF-α协同作用可增加肉鸡外周血淋巴细胞与颈静脉内皮细胞间的黏附,同时高剂量APS(1000 μg/mL)可通过改变血管ICAM-1和T淋巴细胞亚群CD4+的分泌(表达)发挥其免疫调节作用。 相似文献
13.
R. Wells A. Guth M. Lappin S. Dow 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2009,23(2):295-300
Background: Dogs with immune-mediated hemolytic anemia (IMHA) and certain inflammatory diseases are at high risk of developing thromboembolic disease. The presence of anti-endothelial cell autoantibodies (AECA) has been associated with an increased risk of thromboembolism in humans.
Hypothesis: AECA will be detected more often in dogs at risk of thromboembolism than in healthy control animals or dogs with diseases not associated with a higher risk of thromboembolism.
Animals: Ninety-one sick dogs and 22 healthy control dogs.
Methods: Retrospective case-controlled study. Serum was screened for the presence of AECA. Dogs were identified for the study based on the risk of thromboembolism as determined by clinical impression and the underlying disease process. Flow cytometry and normal canine endothelial cells were used to screen serum samples from sick and healthy control dogs for the presence of AECA. In addition, serum from dogs with confirmed thromboemboli was also screened for the presence of AECA by immunohistochemistry.
Results: AECA were detected in 2/91 sick dogs, both with infectious diseases, but were not found in healthy dogs. Anti-endothelial antibodies were not detected in 21 dogs with IMHA and 20 dogs with systemic inflammatory response syndrome, sepsis, or both.
Conclusions: We conclude that AECA are rarely detectable in dogs considered at high risk of thromboembolism. These findings suggest that AECA may not play an important role in the pathogenesis of thromboembolism in dogs with IMHA and other inflammatory diseases. 相似文献
Hypothesis: AECA will be detected more often in dogs at risk of thromboembolism than in healthy control animals or dogs with diseases not associated with a higher risk of thromboembolism.
Animals: Ninety-one sick dogs and 22 healthy control dogs.
Methods: Retrospective case-controlled study. Serum was screened for the presence of AECA. Dogs were identified for the study based on the risk of thromboembolism as determined by clinical impression and the underlying disease process. Flow cytometry and normal canine endothelial cells were used to screen serum samples from sick and healthy control dogs for the presence of AECA. In addition, serum from dogs with confirmed thromboemboli was also screened for the presence of AECA by immunohistochemistry.
Results: AECA were detected in 2/91 sick dogs, both with infectious diseases, but were not found in healthy dogs. Anti-endothelial antibodies were not detected in 21 dogs with IMHA and 20 dogs with systemic inflammatory response syndrome, sepsis, or both.
Conclusions: We conclude that AECA are rarely detectable in dogs considered at high risk of thromboembolism. These findings suggest that AECA may not play an important role in the pathogenesis of thromboembolism in dogs with IMHA and other inflammatory diseases. 相似文献
14.
H Cambridge J A Reynoldson J D Dunsmore B J Hilbert 《Research in veterinary science》1987,42(2):150-153
A radioimmunoassay for thromboxane B2 (TXB2) in unextracted horse plasma was evaluated. Sensitivity of the assay was 14.0 (SD 5.6) pg ml-1 of plasma. Interassay and intra-assay variation were 21.3 per cent and 4.3 per cent, respectively. The percentage of tracer bound in unextracted plasma in the absence of TXB2 was often higher than that in buffer. Therefore standard curves were obtained using standards diluted in plasma from horses treated with aspirin or in charcoal treated TXB2-free plasma. Standard curves determined in plasma and buffer were parallel. This assay was used to determine the half-life of exogenous TXB2 in horses. The mean value of 20.7 minutes (n = 3) is similar to that determined in other species. Storage of plasma samples at -20 degrees C for four months was found to alter the TXB2 levels in an unpredictable manner. Mean recovery was 102.4 per cent (SD 44.1). Effect of variability in sample collection and handling was assessed, but no consistent source of artifactual generation of TXB2 was found. 相似文献
15.
The effect of lipopolysaccharide on ovine endometrial tissue was examined at estrus (follicular phase) and during the luteal phase. Endometrial tissues were cultured with 0, 1, or 10 microg/mL lipopolysaccharide. After 24 h, culture supernates were harvested and analyzed for PGF2alpha, PGE2, 6-keto-PGF1alpha, thromboxane B2 (TXB2), and cysteinyl-leukotrienes (leukotrienes) using EIA. Homogenates of endometrial tissue were analyzed for prostaglandin endoperoxidase-1 (PTGS-1), and -2 (PTGS-2) as well as Type-I, -II, and -III nitric oxide synthase (NOS) by Western analysis. Follicular phase tissue produced more PGF2alpha (P < 0.001), TXB2 (P < 0.001), and leukotrienes (P < 0.02) than luteal tissue. Lipopolysaccharide increased PGE2 (P < 0.001) and TXB2 (P < 0.02) production by endometrial tissue. Elevations in these eicosanoids were likely due to the measured increases in PTGS-2 (P = 0.002) because no changes in PTGS-1 (P = 0.54) or Type-I, -II, or -III NOS (P > or = 0.20) occurred in endometrial tissue following lipopolysaccharide exposure. These data suggest that the phase of the estrous cycle regulates prostaglandin production by immune-challenged endometrial tissue. 相似文献
16.
M G O'Sullivan L N Fleisher N C Olson N J MacLachlan T T Brown 《American journal of veterinary research》1990,51(11):1820-1825
Stimulation of bovine alveolar macrophages with calcium ionophore A23187 resulted in marked production of leukotriene (LT)B4 and a lesser increase in thromboxane (TX)B2, whereas opsonized zymosan (OPZ) resulted in production of TXB2 and relatively small increases in LTB4 and prostaglandin (PG)F2 alpha. Alveolar macrophages incubated with recombinant bovine interferon-gamma or lipopolysaccharide, and subsequently stimulated with A23187 or OPZ, had altered arachidonic acid metabolism, producing markedly increased amounts of TXB2 and PGF2 alpha, and slightly increased LTB4. Incubation of alveolar macrophages with lipopolysaccharide had a more profound effect on the increased amounts of TXB2 and PGF2 alpha, observed in response to stimulation with A23187 or OPZ, than did incubation with interferon-gamma. Alveolar macrophages incubated with recombinant bovine interferon-alpha 1-1 also produced slightly increased amounts of LTB4 when stimulated with A23187 or OPZ. Altered arachidonic acid metabolism by alveolar macrophages exposed to interferons and lipopolysaccharide may contribute to the development of pulmonary inflammation, such as in the early stages of bacterial pneumonia following viral infections that induce interferon production. 相似文献
17.
Jones CJ Streppa HK Harmon BG Budsberg SC 《American journal of veterinary research》2002,63(11):1527-1531
OBJECTIVE: To evaluate in vivo activity in dogs of meloxicam or aspirin, previously shown in vitro to be a selective cyclooxygenase-2 (COX-2) inhibitor (COX-1 sparing drug), or a nonselective COX inhibitor, respectively. ANIMALS: 12 male dogs with unilateral osteoarthritis of the stifle joint. PROCEDURE: Each dog was treated in a crossover design with aspirin or meloxicam for 21 days. Prostaglandin E2 (PGE2) concentrations were measured at days 0 (baseline), 7, and 21 of each treatment period in lipopolysaccharide (LPS)-stimulated blood, synovial fluid collected by arthrocentesis, and endoscopic gastric mucosal biopsy specimens. Thromboxane B2 (TXB2) was evaluated in blood on days 0, 7, and 21 of each treatment period. RESULTS: Aspirin administration significantly suppressed PGE2 concentrations in blood, gastric mucosa, synovial fluid, and suppressed TXB2 concentration in blood at days 7 and 21. Meloxicam administration significantly suppressed PGE2 concentrations in blood and synovial fluid at days 7 and 21, but had no effect on concentrations of TXB2 in blood or PGE2 in gastric mucosa. Suppression of LPS-stimulated PGE2 concentrations in blood and synovial fluid by aspirin and meloxicam administration is consistent with activity against the COX-2 isoenzyme. Suppression of concentrations of PGE2 in the gastric mucosa and TXB2 in blood by aspirin administration is consistent with activity against COX-1. Meloxicam, in contrast, had a minimal effect on functions mediated by COX-1. CONCLUSIONS AND CLINICAL RELEVANCE: Meloxicam acts in vivo in dogs as a COX-1 sparing drug on target tissues by sparing gastric PGE2 synthesis while retaining antiprostaglandin effects within inflamed joints. 相似文献
18.
嗜水气单胞菌粘附特性的研究 总被引：7，自引：1，他引：6
不同来源的６株嗜水气单胞菌（Ａｅｒｏｍｏｎａｓｈｙｄｒｏｐｈｉｌａ）对１０种不同红细胞的血凝试验表明，Ｊ－１株能凝集所有的１０种红细胞，而与其他菌株的血凝谱有所不同。血凝图式有２种：人、鸡、麻雀的红细胞凝集快，呈大小不等的絮状；而鲫鱼、绵羊、猪、小鼠、兔、鸭、犬的红细胞凝集慢，且呈均匀颗粒状。这两种血凝均能被Ｄ－甘露糖抑制，但不能被Ｊ－１株Ｒ菌毛抑制。组织粘附试验显示，Ｊ－１株能粘附小鼠和鲫鱼的肠组织和肠绒毛。将提纯的Ｒ菌毛预处理肠组织，或用Ｄ－甘露糖或木瓜蛋白酶消化的Ｒ菌毛抗血清Ｆａｂ片段预处理菌体，都不能抑制上述的粘附作用。Ｊ－１株对ＨＥｐ－２细胞显示强粘附，菌体随机粘附在细胞上，有少数侵入细胞浆内。其余５株菌的粘附特性与Ｊ－１株不尽相同。所有６株菌对草鱼肠组织及肠绒毛、ＥＰＣ细胞（鲤鱼乳头状上皮瘤细胞系）均无粘附性。 相似文献
19.
J A Stick W A Arden R A Robinson E M Shobe R A Roth 《American journal of veterinary research》1992,53(4):563-568
Effects of 1 hour of colonic volvulus and 3 hours of reperfusion on concentrations of thromboxane (TXB2) and prostacyclin (6-keto-PGF1 alpha) in portal, pulmonary arterial, and jugular blood were determined by radioimmunoassay to assess the site of production and clearance of these eicosanoids from the circulation in 5 anesthetized ponies. Colonic volvulus had no significant effect on mean arterial pressure or TXB2 concentrations, but significantly (P less than 0.05) increased 6-keto-PGF1 alpha concentrations in all blood samples. Immediately after colonic reperfusion, all eicosanoid concentrations were significantly (P less than 0.05) increased. Then, TXB2 returned to baseline values, whereas 6-keto-PGF1 alpha concentrations remained significantly (P less than 0.05) high for the remainder of the study. Eicosanoid concentrations were significantly (P less than 0.05) greater in portal blood than in pulmonary arterial and jugular blood samples at all periods. This suggests that the splanchnic circulation is the primary site of eicosanoid production during and after colonic volvulus and the liver appears to provide most of the circulatory clearance of thromboxane and prostacyclin. 相似文献
20.
OBJECTIVE: To evaluate in vivo activity of carprofen, deracoxib, and etodolac on prostanoid production in several target tissues in dogs with chronic osteoarthritis. ANIMALS: 8 dogs with chronic unilateral osteoarthritis of the stifle joint. PROCEDURE: Each dog received carprofen, deracoxib, or etodolac for 10 days with a 30- to 60-day washout period between treatments. On days 0, 3, and 10, prostaglandin (PG) E2 concentrations were measured in lipopolysaccharide-stimulated blood, synovial fluid, and gastric mucosal biopsy specimens; PGE1 concentrations were measured in gastric mucosal biopsy specimens; and thromboxane B2 (TXB2) was evaluated in blood. RESULTS: Carprofen and deracoxib significantly suppressed PGE2 concentrations in blood at days 3 and 10, compared with baseline, whereas etodolac did not. None of the drugs significantly suppressed TXB2 concentrations in blood or gastric PGE1 synthesis at any time point. All 3 drugs significantly decreased gastric synthesis of PGE2 at day 3 but not day 10 of each treatment period. All 3 drugs decreased synovial fluid PGE2 concentrations in the affected and unaffected stifle joints at days 3 and 10. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that carprofen and deracoxib act in vivo on target tissues as COX-1-sparing drugs by sparing gastric PGE1 and PGE2 synthesis and production of TXB2 by platelets. Etodolac also appears to be COX-1 sparing but may have variable effects on COX-2 depending on the tissue. In gastric mucosa and synovial fluid, there were no significant differences in PG production between compounds at recommended concentrations. 相似文献