青天葵提取物对小鼠急性肺损伤的保护作用

为探讨青天葵乙酸乙酯提取物对小鼠急性肺损伤(acute lung injury,ALI)的保护作用,本试验选择50只昆明小鼠随机分为模型组、青天葵(高、中、低)治疗组和空白对照组,采用内毒素腹腔注射法建立急性肺损伤模型。观察肺脏湿/干重比(W/D)、病理切片、肺脏组织匀浆中丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(SOD)的含量变化。结果发现,青天葵乙酸乙酯提取物可以明显减轻损伤肺脏组织的形态学变化,肺脏组织匀浆中MDA、SOD与模型组相比差异极显著,证实青天葵乙酸乙酯提取物对小鼠急性肺损伤具有保护作用。     

银杏内酯A对LPS诱导的小鼠急性肺损伤的保护作用

为了研究银杏内酯A对非特异性肺损伤小鼠的保护作用,采用脂多糖（LPS）滴鼻法建立了小鼠急性肺损伤（ALI）模型。于造模前1h给予银杏内酯A（50,100mg/kg）,在LPS滴入后18h检测支气管肺泡灌洗液（BALF）中的细胞因子TNF-α、IL-6、IL-1β水平,观察肺部组织学的病理变化。结果表明：银杏内酯A可以显著抑制肺组织中炎性细胞的浸润,抑制肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）和白细胞介素1β（IL-1β）炎性细胞因子的产生。由此得出结论,银杏内酯A对LPS诱导的小鼠ALI具有一定的保护作用。     

迷迭香酸对哮喘小鼠氧化性肺损伤的保护作用

为评价迷迭香酸对哮喘小鼠模型氧化性肺损伤的保护作用,本研究用卵清蛋白（OVA）致敏、激发雌性BALB/c小鼠建立哮喘模型,并用OVA和H₂O₂联合激发小鼠作为氧化肺损伤阳性对照模型。在最后一次滴鼻激发24 h后,取支气管肺泡灌洗液（BALF）进行细胞计数并测定活性氧（ROS）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）水平,取左侧肺脏固定做HE染色。结果显示,迷迭香酸可明显减少BALF中细胞总数和嗜酸性粒细胞数目,显著抑制肺组织和BALF中ROS的产生,升高SOD和GSH-Px水平,改善肺组织病理变化。本试验结果表明,迷迭香酸对氧化肺损伤起到明显的保护作用。     

谷氨酰胺复合胶囊对小鼠CCL_4肝损伤的保护作用

目的:研究了谷氨酰胺复合胶囊对小鼠CCL_4肝损伤的保护作用。方法:选取实验室中心同一批培养的30只SD小鼠,随机分为正常组、对照组与观察组。正常组小鼠不进行任何干预,对照组小鼠以5mL/kg的剂量腹部注射1%CCL_4油溶液建立模型,观察组小鼠在建立模型后每天给予谷氨酰胺复合胶囊治疗。观察三组血清ALT、AST的变化。结果:对照组血清ALT、AST明显高于正常组(P<0.05),观察组ALT、AST虽然高于正常组(P<0.05),但是明显低于对照组(P<0.05)。结论:谷氨酰胺复合胶囊能够有效改善CCL_4肝损伤小鼠的肝功能状况。     

橄榄苦苷对脂多糖诱导的急性肺损伤小鼠的保护作用

为了探讨橄榄苦苷对脂多糖(LPS)诱导的急性肺损伤小鼠的保护作用,选用80只健康昆明系小鼠分成正常对照组、模型组、地塞米松组和橄榄苦苷组。结果显示,橄榄苦苷能减少炎症细胞浸润,使肺泡壁增厚减轻;能降低血清中肿瘤坏死因子α(TNF-α)、细胞间粘附分子-1(ICAM-1)、白细胞介素6(IL-6)的含量(P0.05,P0.01);能提高肺组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)活性,降低丙二醛(MDA)的含量(P0.01);能提高肺组织闭锁蛋白表达水平(P0.01)。说明橄榄苦苷对LPS诱导的急性肺损伤具有明显的保护作用,其机制可能与减少自由基损伤、抑制炎症因子水平及提高肺组织细胞连接蛋白的表达有关。     

蒲公英对急性肺损伤小鼠的保护作用

急性肺损伤(ALI)是指由肺内外致病因素导致的急性进行性缺氧性呼吸衰竭,是一种常见而严重的呼吸急症,目前尚无特效的治疗措施,药物治疗常用糖皮质激素,其疗效并不很理想.蒲公英作为一种传统的中药,临床主要用于乳痈、咽痛、热淋涩痛等症的治疗.本试验通过脂多糖(LPS)诱导小鼠建立模型,从抗炎角度研究其对ALI小鼠是否具有保护作用,为蒲公英的临床应用和深入研究提供依据.     

穿王消炎粉对LPS诱导大鼠急性肺损伤的治疗作用

【目的】 研究穿王消炎粉对脂多糖(LPS)诱导大鼠急性肺损伤(ALI)的治疗作用。【方法】 将60只SD雄性大鼠随机分入空白组、左氧氟沙星阳性药物对照组、LPS模型组及穿王消炎粉低(1 g/kg体重)、中(2 g/kg体重)、高(4 g/kg体重)剂量组,每组10只。模型组和给药组大鼠经滴鼻法给予LPS(3 mg/kg体重)制备大鼠ALI模型,24 h后,给药组分别灌胃相应浓度的穿王消炎粉,模型组和空白组灌胃相同体积的生理盐水。治疗4 d后处死大鼠,分离血清、固定并冻存肺脏组织。测定各组大鼠肺脏组织湿/干重比;HE染色观察大鼠肺脏组织病理学变化;ELISA法检测血清中白细胞介素-1β(IL-1β)、IL-6含量;采用实时荧光定量PCR和Western blotting法检测肺脏组织中IL-1β、IL-6 mRNA表达水平和蛋白表达量。【结果】 与空白组相比,LPS模型组大鼠出现肺间质壁增厚,肺泡腔内炎性细胞浸润、出血,肺泡结构破坏等肺损伤症状,肺组织的湿/干重比极显著升高(P<0.01),血清中IL-1β、IL-6含量和肺脏组织中IL-1β、IL-6 mRNA表达水平及蛋白表达量均显著增加(P<0.05)。与LPS模型组相比,各给药组大鼠肺间质增宽现象有所改善,肺组织的湿/干重比、血清和肺脏组织中炎性因子IL-1β、IL-6 mRNA表达水平及蛋白表达量均显著降低(P<0.05)。【结论】 穿王消炎粉可有效抑制LPS诱导的急性肺部损伤和炎症程度。     

胆酸对LPS诱导小鼠乳腺炎的保护作用及其机制

乳腺炎是危害奶牛养殖业最为主要的疾病之一,严重制约着奶业的健康发展。抗生素作为乳腺炎的主要治疗药物,易造成细菌耐药性等问题。因此,寻找安全有效的方法或制剂替代抗生素对于乳腺炎的防治具有重要意义。胆酸(cholic acid, CA)作为机体的天然代谢产物,报道具有抑菌抗炎功能。本研究旨在探讨CA对脂多糖(LPS)诱导小鼠乳腺炎的保护作用及机制。将40只分娩后的BALB/c母鼠随机分为5组,包括空白对照组、LPS造模组、LPS+CA(10 mg/kg)组、LPS+CA(20 mg/kg)组和LPS+CA(30 mg/kg)组。通过对小鼠乳腺组织进行病理学观察、炎性细胞因子及相关信号通路检测等方法探究CA对LPS诱导小鼠乳腺炎的保护作用及机制。结果显示,CA呈剂量依赖性地改善LPS诱导小鼠乳腺组织病理损伤,显著降低髓过氧化物酶(MPO)活性和炎性细胞因子TNF-α和IL-1β的表达。进一步研究表明,CA显著抑制了LPS诱导的NF-κB信号通路激活,增加了法尼醇X受体(FXR)的表达。结果表明,CA通过上调FXR受体表达,进而抑制LPS诱导的NF-κB信号通路及炎性细胞因子产生,发挥对乳腺炎...     

参麦注射液对大鼠急性肺损伤保护作用及机制的研究

试验旨在探讨参麦注射液对大鼠肺组织的保护作用及可能机制,为临床治疗急性肺损伤(acute lung injury,ALI)提供理论依据。将Wister大鼠随机分为模型组、参麦治疗组和空白对照组,每组采用经典尾静脉注射油酸方法建立急性肺损伤模型。观察肺体系数、病理切片、超微结构及肺组织匀浆中TNF-α、ICAM-1的含量变化,探讨参麦注射液对大鼠肺组织急性肺损伤的保护作用。结果发现,与模型组相比参麦治疗组可以明显改变大鼠急性肺损伤的肺体系数,减轻肺组织形态学及超微结构的病理改变,同时降低肺组织匀浆中TNF-α、ICAM-1的表达。证实参麦注射液对大鼠急性肺损伤具有保护作用,其机制可能通过降低肺组织匀浆中TNF-α、ICAM-1的含量,而发挥抗炎作用。     

芹菜素对小鼠急性肺损伤的保护作用

急性肺损伤是由创伤、感染、休克等诸多非心源性因素导致的一种急性、进行性呼吸障碍。该病的主要特点是出现顽固型低氧血症、促进呼吸频数升高、呼吸加重、呼吸困难、X线分析结果显示肺泡多出现弥漫性浸润等。本实验在构建LPS诱导的小鼠急性肺损伤模型的基础上,通过观察肺组织病理学变化、肺组织MPO活性变化及炎性细胞数量、促炎性细胞因子及NF-κB和MAPKs信号通路中关键接头蛋白分子磷酸化水平变化,探讨芹菜素对LPS诱导的小鼠急性肺损伤的保护作用。     

肠道微生物对流感病毒感染小鼠肺损伤调节作用的研究

流感病毒作为一种常见的呼吸道病毒,是人类健康和世界经济的巨大威胁。目前流感治疗遇到病毒高度突变的问题,不断完善已有的控制流感感染方法的同时,也需要开阔视野从宿主反应的角度探索控制流感的新措施,本研究从肠道微生物的角度探索流感造成肺损伤的机制。提前3周将组合抗生素和益生元添加到小鼠饮水中构建不同的肠道微生物环境,小鼠感染流感病毒后运用16S rDNA技术测定结肠微生物组成,蛋白免疫印迹法测定肺部Th17和Treg细胞转录因子RORγT和Foxp3的表达情况,苏木精-伊红染色、荧光定量PCR测定肺损伤状况。结果表明,提前使用组合抗生素和益生元能够改变肠道菌群组成,通过降低肠道菌群数目和增加肠道拟杆菌相对丰度保护肠道,从而反作用于肺部诱导肺Treg细胞分化,抑制Th17细胞分化,改善流感造成的肺损伤。     

Expression of secreted mucins (MUC2, MUC5AC, MUC5B, and MUC6) and membrane-bound mucin (MUC4) in the lungs of pigs experimentally infected with Actinobacillus pleuropneumoniae

The expression patterns of different secreted (MUC2, MUC5AC, MUC5B, and MUC6) and membrane-bound (MUC4) mucins were determined immunohistochemically in the lungs of pigs experimentally infected with Actinobacillus pleuropneumoniae. Forty-seven-week-old colostrum-deprived pigs were randomly allocated to infected (n=20) or control groups (n=20). Five infected and uninfected pigs were euthanized at 0, 6, 12, and 48 h post-inoculation (hpi). In the infected pigs, the expression of both types of mucins, which were invariably observed, was associated with bronchiolar and respiratory bronchiolar lesions. Strong positive mucin signals were seen on the surface of bronchiolar and respiratory bronchiolar epithelium with neutrophil infiltration. The mean mucin-positive area peaked at 6 hpi and decreased significantly to control levels by 48 hpi on the surface of the bronchiolar and respiratory bronchiolar epithelium. Further studies are needed to establish the functional relationship between mucin expression and the host defense mechanism against A. pleuropneumoniae in the lungs of infected pigs.     

急性热应激对小鼠肺组织中热应激蛋白和细胞因子基因表达的影响

为研究小鼠在急性热应激条件下肺组织中几种热应激蛋白(heat shock proteins,HSPs)及一些细胞因子基因表达水平的变化情况,通过实时荧光定量PCR的方法检测小鼠急性热应激前后肺组织中HSP27、HSP60、HSP70、HSP90、HSP110及白细胞介素-6(IL-6)、白细胞介素-17(IL-17)、肿瘤坏死因子α(TNF-α)、β干扰素(IFN-β)及γ干扰素(IFN-γ)的mRNA水平变化情况。结果显示,所有检测的热应激蛋白和细胞因子在热应激后0 h至2h过程中均极显著升高(P0.01),到4 h时恢复到正常水平。此试验结果为揭示急性热应激提高机体的抗病能力提供有价值的资料。     

Differential association of MUC5AC and CLCA1 expression in small cartilaginous airways of RAO‐affected and control horses

Reasons for performing study: Airway mucus accumulation is associated with indoor irritant and allergen exposure in horses with recurrent airway obstruction (RAO). Epidermal growth factor receptor (EGFR) and a chloride channel (calcium activated, family member 1; CLCA1) are key signalling molecules involved in mucin gene expression. Objectives: We hypothesised that exposure to irritants and aeroallergens would lead to increased expression of the mucin gene eqMUC5AC and increased stored mucosubstance in the airways of RAO‐affected horses, associated with increased neutrophils and CLCA1 and EGFR mRNA levels. Methods: We performed quantitative RT‐PCR of eqMUC5AC, CLCA1 and EGFR; volume density measurements of intraepithelial mucosubstances; and cytological differentiation of intraluminal inflammatory cells in small cartilaginous airways from cranial left and right and caudal left and right lung lobes of 5 clinically healthy and 5 RAO‐affected horses that had been exposed to indoor stable environment for 5 days before euthanasia. Results: Neutrophils were increased in RAO‐affected horses compared to clinically healthy controls. EqMUC5AC mRNA levels were positively correlated with both CLCA1 and EGFR mRNA levels in RAO‐affected horses but only with CLCA1 in controls. The relationship between eqMUC5AC and CLCA1 differed in the 2 groups of horses with RAO‐affected animals overexpressing CLCA1 in relation to eqMUC5AC. Conclusions: These data implicate CLCA1 as a signalling molecule in the expression of eqMUC5AC in horses but also suggest differential regulation by CLCA1 and EGFR between horses with RAO and those with milder degrees of airway inflammation.     

栀子苷对小鼠哮喘的保护作用及其机制

通过Ova（鸡卵清蛋白）诱导和激发BALB/c小鼠,构建哮喘疾病动物模型,探究栀子苷对非感染性气道炎症的调控作用,并探讨其可能的作用机制。研究发现,栀子苷（80mg/kg）可显著调节Ova触发的哮喘症状,如减少BALF中嗜酸性粒细胞数和炎性细胞总数;下调BALF（支气管肺泡灌洗液）中Th2细胞因子IL-4、IL-5和IL-13及嗜酸性趋化因子水平;降低血清中Ova特异性IgE的含量;改善支气管周围肺组织病理学变化和气道高反应性等。结果表明,栀子苷可通过缓减炎症过程保护Ova致小鼠过敏性哮喘,其机制可能与阻断NF-κB（核转录因子-κB）信号转导通路的激活有关,为栀子苷在治疗哮喘等疾病及相关原料药物研发过程提供理论和数据支持。     

大蒜多糖对ConA致小鼠肝损伤保护作用组织学观察

探讨大蒜多糖（GPA）对刀豆蛋白A（ConA）诱导的小鼠免疫性肝损伤的保护作用和对肝糖原的影响。将40只小鼠随机分为5组,即空白对照组、模型组、不同剂量多糖组（100、200、400mg／kg）。空白对照组和模型组小鼠灌胃生理盐水,多糖组小鼠分别以相应剂量灌胃,至第7天处死前8h,除空白对照组外所有小鼠尾静脉注射ConA,以制造急性免疫性肝损伤,取肝组织,进行病理学观察。结果模型组小鼠肝组织变性、坏死、瘀血等损伤严重,细胞界线与细胞核模糊不清,肝糖原含量减少,多糖组小鼠肝组织损伤均明显较轻,肝细胞界线清晰,糖原含量减少不显著,100mg／kg多糖组接近正常水平。研究表明,大蒜多糖能够促进肝糖原合成和储存,对小鼠免疫性肝损伤有良好的保护作用。     

Immunogenicity and protective effects of truncated recombinant leukotoxin proteins of Fusobacterium necrophorum in mice

Fusobacterium necrophorum, a gram-negative, anaerobic and rod-shaped bacterium, is generally an opportunistic pathogen and causes a wide variety of necrotic infections in animals and humans. Leukotoxin, a secreted protein, is a major virulence factor. The gene encoding the leukotoxin (lktA) in F. necrophorum has been cloned, sequenced and expressed in Escherichia coli. Because of low expression levels, problems associated with purifying full-length recombinant protein, and of the physical instability of the protein, five overlapping leukotoxin gene truncations were constructed. The recombinant polypeptides (BSBSE, SX, GAS, SH, and FINAL) were expressed in E. coli and purified by nickel-affinity chromatography. The objectives were to investigate the effectiveness of the purified truncated polypeptides to induce protective immunity in mice challenged with F. necrophorum. The polypeptides, individually or in combination, and inactivated native leukotoxin or culture supernatant of F. necrophorum were homogenized with an adjuvant and injected into mice on days 0 and 21. Blood samples were collected to measure serum anti-leukotoxin antibody titers on days 0, 21 and 42 and on day 42, mice were experimentally challenged with F. necrophorum. All polypeptides were immunogenic, with GAS polypeptide eliciting the least antibody response. Two polypeptides (BSBSE and SH) induced significant protection in mice against F. necrophorum infection. Protection was better than the full-length native leukotoxin or inactivated supernatant.The study demonstrated that the leukotoxin of F. necrophorum carries epitopes that induce protective immunity against experimental fusobacterial infection, thus providing further evidence to the importance of leukotoxin as a major virulence factor.     

谷氨酰胺对断奶仔猪肝脏SOD、GSH-Px基因表达的影响

选用60头21日龄断奶杜长大仔猪,随机分为2组,每组设3个重复,每个重复10头。试验组在基础日粮中添加0.5%谷氨酰胺（Gln）分别于断奶后0、7、14d屠宰采样,采用相对定量RT-PCR方法检测添加Gln对仔猪肝脏中超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）mRNA表达水平的影响。结果表明：断奶后7d,0.5%Gln试验组肝脏SOD酶活力比对照组低6.93%（P〉0.05）,GSH-Px酶活力比对照组高11.87%（P〈0.05）;断奶后14d,0.5%Gln组SOD酶活力比对照组低9.54%（P〉0.05）,GSH-Px酶活力比对照组高9.56%（P〈0.05）。与对照组相比,试验组SOD基因表达量减少,而GSH-Px增加。在断奶后7、14d,仔猪肝脏SODmRNA表达量分别降低了47.94%（P〉0.05）和77.02%（P〈0.05）;GSH-PxmRNA表达量分别提高了73.16%（P〈0.05）和28.27%（P〉0.05）。