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1.
采用组织化学和免疫组化的染色方法,检测趾叶炎小鼠趾部组织中肿瘤坏死因子(TNF-α)的表达水平、炎性细胞、肥大细胞及其脱颗粒的动态变化.结果显示,造模组在免疫后14 d TNF-α表达达到一个峰值,而后表达开始减弱,21 d后表达开始增强,极显著高于同一时相正常组(P<0.01);各治疗组其表达均极显著低于同一时相造模组,其中低剂量治疗组小鼠同一时相均极显著高于正常组(P<0.01),中剂量治疗组小鼠除免疫后前3个时相显著外(P<0.05),免疫后35 d与正常组不显著(P>0.05),高剂量治疗组小鼠除免疫后14 d显著外(P<0.05),其余各时相均与正常组不显著(P>0.05),各治疗组小鼠的TNF-α表达水平并随药物浓度的提高和免疫时间的延长而逐渐减弱,而肥大细胞及其脱颗粒和炎性细胞变化均与TNF-α的表达趋势相吻合.结果表明,Mizolastine可以显著抑制TNF-α的表达.  相似文献   

2.
应用组织化学方法及免疫组化技术对正常组和急性攻毒组大鼠生殖器官中肥大细胞的活性以及P物质表达水平的动态变化进行了研究.结果表明:攻毒后6小时子宫和卵巢炎性细胞、肥大细胞及其脱颗粒数量达到峰值,而后开始减少,48~72 h又开始回升,其中炎性细胞均极显著高于攻毒前(P<0.01);肥大细胞除子宫攻毒后12小时(P<0.05),其余均极显著高于攻毒前(P<0.01);肥大细胞脱颗粒数攻毒后6小时、72小时显著高于攻毒前(P<0.05),且在攻毒后72小时子宫内膜和6小时卵巢皮质的小血管内皮细胞均出现轻微脱落损伤;同时不同时相P物质表达的趋势与炎性细胞、肥大细胞及其脱颗粒数量变化相吻合,且P物质神经纤维与肥大细胞相关联.说明在乳腺炎中P物质、肥大细胞影响生殖.  相似文献   

3.
应用组织化学方法及免疫组化技术对正常组和急性攻毒组大鼠乳腺肥大细胞的数量、活性、组化性质以及P物质表达水平的动态变化进行了研究。结果表明:急性攻毒6小时大量炎性细胞浸润在乳腺小叶间质、腺泡间、腺泡腔内及血管周围,且达到最高峰,之后又开始减少,48~72小时开始上升,小叶间质内的小血管内皮细胞开始出现裂隙、脱落损伤;乳汁蛋白在攻毒后6小时开始减少,以后分泌开始逐渐增多;同时不同时相肥大细胞的脱颗粒数及P物质表达水平均与炎性细胞的浸染变化相吻合,且攻毒后肥大细胞和其脱颗粒数均显著高于攻毒前(P(0.05),表明P物质的表达水平并与肥大细胞相关联。说明P物质和肥大细胞参与大鼠乳腺炎的发病过程。  相似文献   

4.
应用组织化学和免疫组织化学方法对正常及攻毒不同时相组大鼠肾组织肥大细胞的数量、活性、分布范型、组织化学性质的动态变化及P物质的表达水平进行了研究。结果显示,攻毒后第6h炎性细胞开始浸染肾小管基膜、肾小囊壁层及肾小球,12h后浸染程度开始减少,第24h出现最低值,而后又开始增多,至第72h浸染达到高峰。且此间质内血管出现轻微的裂隙。同时不同时相肾组织的肥大细胞及其脱颗粒数量和P物质的表达水平均与炎性细胞浸染变化相吻合,攻毒后第6、12、48、72h的炎性细胞、肥大细胞及其脱颗粒数量均显著高于攻毒前(P〈0.05),且在攻毒后第72h均达到最高值;P物质的表达与肥大细胞相关联。证实,肥大细胞和P物质参与了乳腺炎所致肾组织损伤与肾功能衰竭的病理过程。  相似文献   

5.
应用组织化学的方法,对正常及攻毒不同时相大鼠肺组织肥大细胞的数量、活力、分布范型和组化性质的动态变化进行了研究.结果表明,攻毒后大量的炎性细胞浸润肺泡隔、细支气管及肺小血管内壁和周围.并随攻毒时间的延长,急剧增多,均极显著高于攻毒前(P<0.01),且在攻毒后24h达到最高峰,此时造成肺小血管的内皮细胞偶见脱落;同时不同时相肺组织肥大细胞及其脱颗粒的变化趋势与炎性细胞相吻合,除攻毒后12h为显著外(P<0.05),二者其余均极显著高于攻毒前(P<0.01).表明肥大细胞参与乳腺炎病理过程中所致肺组织损伤的病理进程.  相似文献   

6.
家畜蹄叶炎是蹄真皮急性、亚急性和慢性弥散性炎症,可侵害几个指(趾),呈现局部和全身性症候.既可以是原发性的,也可能继发于其他疾病.到目前为止,发病原因说法不一,国内外学者多认为主要致病因素是毒素、组织胺和代谢紊乱.家畜患蹄叶炎时真皮血管系统受到侵害,导致指(趾)部毛细血管血液灌流量减少,造成局部缺血,这种血管变化在早期非常清楚,并且最早的病理变化是停滞性氧不足.  相似文献   

7.
实验性乳腺炎小鼠乳腺肥大细胞的变化   总被引:1,自引:0,他引:1  
应用改良甲苯胺蓝染色法和苏木精-伊红染色法对金黄色葡萄球菌诱发实验性乳腺炎小鼠乳腺肥大细胞的数量、分布、活性进行了研究。正常对照组小鼠乳腺组织中肥大细胞主要分布于乳腺小叶之间的结缔组织中,有些围绕血管或乳腺导管分布,腺上皮之间没有肥大细胞分布;阳性试验组小鼠乳腺肥大细胞主要分布在相邻腺泡周围或腺导管上皮周围,胞质内充满异染颗粒,脱颗粒状态显著,甚至表现有颗粒耗竭现象,腺泡中有一定程度的肥大细胞浸润。肥大细胞计数结果显示,阳性试验组母鼠乳腺内的肥大细胞数急剧增多,显著高于正常对照组(P<0.05),而脱颗粒肥大细胞数阳性试验组与正常对照组相比极显著增多(P<0.01)。结论:肥大细胞在小鼠乳腺炎的致病机制中发挥重要作用,参与了乳腺炎的发病过程。  相似文献   

8.
一、发病原因1.精料喂的过多,而又缺乏草料,瘤胃内产生大量乳酸,瘤胃内环境的破坏可使胃黏膜抵抗力下降,屏障作用减弱,使有毒物质进入循环系统。此外,在瘤胃发生炎症的情况下,肥大细胞脱颗粒而释放组织胺,这些都可诱发蹄叶炎。  相似文献   

9.
一、发病原因 1.精料喂的过多,而又缺乏草料,瘤胃内产生大量乳酸,瘤胃内环境的破坏可使胃黏膜抵抗力下降,屏障作用减弱,使有毒物质进入循环系统。此外,在瘤胃发生炎症的情况下,肥大细胞脱颗粒而释放组织胺,这些都可诱发蹄叶炎。  相似文献   

10.
为探究金荞麦对脂多糖(LPS)诱导的小鼠小肠炎症的保护作用,试验使用雌性ICR小鼠,前期14 d饮水添加不同浓度金荞麦和阳性对照品——芦丁(Rutin),随后腹腔注射LPS(10 mg/kg)构建小肠急性炎症模型,通过观察小鼠行为变化、血常规检测、组织切片和炎症相关基因定量检测等评估效果。结果发现,腹腔注射10 mg/kg的LPS可成功诱导小鼠急性肠炎;添加金荞麦能够剂量依赖性地降低LPS诱导的肠炎小鼠体重损失。血常规检测显示,腹腔注射LPS后导致小鼠血液白细胞数(WBC)、红细胞数(RBC)、血红蛋白(HGB)、血小板数目(PLT)显著下降,添加金荞麦或芦丁能一定程度缓解由于LPS引起的血常规异常。小肠切片HE染色结果显示,腹腔注射LPS后小肠固有层中间出现大量灶性的炎性细胞浸润,腺上皮可见少量的炎性细胞浸润,肠道细胞排列紊乱,可见核分裂及核碎裂,同时黏膜充血、出血严重;添加金荞麦或芦丁能一定程度抑制炎性细胞浸润和黏膜出血。实时荧光定量PCR结果显示,腹腔注射LPS能显著促进小肠促炎性因子IL-6、TNF-α和IL-1β的表达,添加金荞麦能剂量依赖性下调TNF-α和IL-1β的表达水平。以上结果表明饮水添加金荞麦和芦丁可以有效缓解LPS诱导的小鼠小肠炎症,金荞麦浓度为12%的添加剂量在部分指标上可达到或接近灌胃100 mg/kg芦丁的效果。  相似文献   

11.
This study investigated the in vitro effect of Lactobacillus strains, a major group of probiotic lactic acid bacteria, on immunoglobulin E (IgE)‐ and antigen‐induced mast cell degranulation and subsequent gene expression. Bone marrow‐derived mast cells (BMMCs) from DBA/2 mice were cultured with heat‐killed Lactobacillus strains for 24 h. Some strains significantly inhibited IgE‐ and antigen‐induced β‐hexosaminidase release from BMMCs. Furthermore, Lactobacillus reuteri NBRC 15892, which exhibited the strongest inhibitory activity, significantly reduced the elevated interleukin (IL)‐4, IL‐13, tumor necrosis factor‐α, and cyclooxygenase‐2 expression levels that was induced by 1–2 h of stimulation with IgE and antigens. The suppressive effect of NBRC 15892 strain on BMMC degranulation was significantly reduced in the presence of a toll‐like receptor (TLR)2‐neutralizing antibody. In addition, downregulation of cell surface FcεRIα expression was observed after 6 h of NBRC 15892 treatment. These results suggest that some Lactobacillus strains inhibited IgE‐mediated mast cell degranulation and subsequent late‐phase reactions involving mast cells via a TLR2‐dependent mechanism with FcεRIα downregulation.  相似文献   

12.
本试验旨在探讨黄芩苷对脂多糖(LPS)诱导的小鼠空肠炎症和氧化应激的缓解作用及其分子机制。将36只小鼠随机分为对照组、阴性对照组、模型组以及低、中、高剂量黄芩苷组,每组6只。适应性生长7 d后开始试验。对照组小鼠不作处理,阴性对照组和模型组小鼠每天灌胃0.2 mL磷酸盐缓冲液(PBS),黄芩苷组小鼠每天灌胃黄芩苷药液0.2 mL(根据小鼠体重计算黄芩苷用量,低剂量组为100 mg/kg BW,中剂量组为200 mg/kg BW,高剂量组为400 mg/kg BW),连续灌胃7 d,第7天给模型组、黄芩苷组小鼠腹腔注射0.2 mL LPS(3.5 mg/kg BW)。注射LPS 24 h后处死小鼠,取空肠进行形态学观察,检测空肠中炎性因子mRNA表达量和含量以及核因子-κB(NF-κB)和核因子-E2相关因子2(Nrf2)/血红素氧合酶-1(HO-1)信号通路关键蛋白表达量的变化。结果显示:相比于对照组,模型组小鼠空肠组织绒毛结构损伤,绒毛高度与隐窝深度比值显著降低(P<0.05),空肠中Toll样受体4(TLR4)的mRNA表达量显著升高(P<0.05),炎性因子[白细胞介...  相似文献   

13.
Hereford heifer calves were experimentally infested with Psoroptes ovis. Histologic examination of skin specimens was conducted at weekly intervals before and after treatment with ivermectin on postinfestation week 7. Electron microscopy revealed numerous degranulating mast cells in the skin of infested but not in control calves. many active, as well as degenerate, neutrophils were in the scab on infested calves. Microscopic epidermal ulcers developed on infested calves when live mites were present but not after treatment. Numbers of dermal neutrophils and plasma cells decreased and numbers of circulating neutrophils increased 1 week after treatment. Numbers of dermal eosinophils and mast cells in calves with eosinophilia increased for several weeks after treatment. Statistical analysis indicated significant correlations (P less than 0.05) among numbers of dermal inflammatory cells, hemogram values, and changes in dermal thickness. Seemingly, mite-induced epidermal damage was the key pathogenic event in psoroptic scabies in calves. Mast cell degranulation contributed to the pathogenesis of the dermatitis, and neutropenia was caused by sustained, poorly compensated efflux of neutrophils into the scab through mite-induced breaks in the epidermis.  相似文献   

14.
将40只雌性ICR小鼠,受孕后随机分为试验组和对照组。雌鼠产后10-11d,试验组经第4对乳头灌注LPS,对照组灌注生理盐水,分别于灌注后不同时间采集样本,组织学分析乳腺病理变化;分析对各组乳腺组织中TLR4和TNF-α mRNA表达变化。组织学结果显示,灌注1.5h后乳腺组织中炎性细胞增多,6、12h乳腺腺泡内有大量的炎性细胞浸润,腺泡结构崩解;6h TLR4 mRNA表达极显著高于对照组(P〈0.01);4个试验组中TNF-αmRNA表达极显著高于对照组(P〈0.01)。试验结果表明LPS能够增强TLR4和TNF-α mRNA表达。  相似文献   

15.
1. Poultry granulocytes are not clearly distinguished from each other with haematoxylineosin (HE) stain; thus, histochemical techniques must be used. Three experiments were carried out using 4-week-old Leghorn chickens. 2. Three, 80-chicken groups were orally infected with (1) 10 8 colony forming units (CFUs) Salmonella enteritidis , or (2) 10 4 Eimeria tenella oocysts, or (3) 10 8 CFUs S. enteritidis + 10 4 E. tenella oocysts. Ten chickens from each group were euthanased and caecum samples obtained. Caecum samples were fixed in 10% formalin (buffered, pH 7.4) at 4, 8, 12 h, 1, 3, 5, 7, and 14 d post-inoculation (PI). 3. Samples were stained using three different staining techniques: HE for the identification of heterophils and eosinophils, Ziehl-Neelsen for mast cells, and p -phenilenediamine dihydrochloride plus pyrocatechol (PPD + PC) for eosinophils. 4. Birds from Experiment 1 showed no changes in the numbers of granulocytes. Birds from Experiments 2 and 3 showed higher numbers of heterophils in caecal mucosa and submucosa separately, on d 5 and 7. In Experiment 3, a decrease was observed in submucosal mast cells on d 3. Chickens from Experiments 2 and 3 showed increased numbers of mucosal mast cells between d 7 and 14. 5. PPD + PC positively stained eosinophils, but not heterophils. 6. Numbers of heterophils and mast cells were increased during the acute inflammatory process caused by E. tenella . Therefore, mast cells could play a role as primary inflammatory cells. Eosinophils seem not to be part of the inflammatory process caused by E. tenella .  相似文献   

16.
The potential role of the mast cells in the invasion of very virulent infectious bursal disease virus (vvIBDV) is unknown. We evaluated mast cell activity and tryptase production after vvIBDV infection in special pathogen-free (SPF) chickens using cytochemistry and immunohistochemistry analyses. The results were as follows: (1) severe histologic lesions were observed in the thymus, spleen, cloacal bursa, liver, kidney and other tissues. vvIBDV viral antigens were detected and presented extensively in the parenchymatous organs, in particular, the cloacal bursa, liver, kidney, thymus, spleen and pancreas. (2) In the vvIBDV-infected group, the mast cell population increased markedly in the liver, kidney, thymus, glandular stomach, spleen and cloacal bursa on days 1, 2 and 3 after vvIBDV infection (p<0.05). However, very few mast cells were observed in those same tissues in the controls, especially in the bursa of Fabricius. (3) Tryptase, a marker for activated mast cells, has a positive correlation with mast cell distribution. The mast cells identified in the tissues were likely to be activated since they were associated with cell degranulation and the presence of tryptase. Furthermore, the co-localization of mast cells, and presence of vvIBDV antigens suggests that the mast cells were activated by vvIBDV infection. Our results also suggest that tryptase may contribute to the inflammation of acute IBD induced by vvIBDV infection. Our research contributes to the further understanding of inflammatory response mechanisms and the contribution of mast cell activity to this process.  相似文献   

17.
The aim of the current study was to determine the possible effects of progestagen oestrous synchronization on vascular endothelial growth factor (VEGF) expression during sheep luteogenesis and the peri‐implantation period and the relationship with luteal function. At days 9, 11, 13, 15, 17 and 21 of pregnancy, the ovaries from 30 progestagen treated and 30 ewes cycling after cloprostenol injection were evaluated by ultrasonography and, thereafter, collected and processed for immunohistochemical evaluation of VEGF; blood samples were drawn for evaluating plasma progesterone. The progestagen‐treated group showed smaller corpora lutea than cloprostenol‐treated and lower progesterone secretion. The expression of VEGF in the luteal cells increased with time in the cloprostenol group, but not in the progestagen‐treated group, which even showed a decrease between days 11 and 13. In progestagen‐treated sheep, VEGF expression in granulosa‐derived parenchymal lobule capillaries was correlated with the size of the luteal tissue, larger corpora lutea had higher expression, and tended to have a higher progesterone secretion. In conclusion, the current study indicates the existence of deleterious effects from exogenous progestagen treatments on progesterone secretion from induced corpora lutea, which correlate with alterations in the expression of VEGF in the luteal tissue and, this, presumably in the processes of neoangiogenesis and luteogenesis.  相似文献   

18.
Recent studies here have demonstrated that increased mast cell populations and tryptase activity contribute to lesion formation in regions of immune organs in special-pathogen-free chickens after infection with very virulent infectious bursal disease virus (vvIBDV). Mast cells and their mediators have been implicated in acute inflammatory injury after vvIBDV infection, but their precise role in this process remains elusive. In this study, the role of mast cells in the vvIBDV infection process was examined using ketotifen, a mast cell membrane stabilizer. On days 1, 2, and 3 postinfection, the bursa of Fabricius (BFs) were collected to quantify mast cells, tryptase and histamine contents by cytochemistry, immunohistochemistry and fluorospectrophotometry analyses, respectively. The results showed that the mast cell populations, tryptase expression, and histamine released increased significantly in the BFs (p < 0.01) of infected birds compared to controls, and acute inflammatory responses were observed in the former. In contrast, in infected chickens pretreated with ketotifen, mast cells, tryptase, and histamine were markedly decreased (p < 0.01) and probably as a result, the BFs remitted significantly. The overall results suggest that mast cells are positively involved in BF injury induced by vvIBDV infection. Inhibition of mast cell degranulation and concurrent mediator release may represent a novel strategy to modulate this process. This study, thus, advances the understanding of the acute inflammatory injury mechanisms triggered by vvIBDV infection and the contribution of mast cell activity in this process.  相似文献   

19.
鼠源重组UBC13蛋白对脂多糖诱导的小鼠急性炎症的影响   总被引:1,自引:1,他引:0  
试验旨在探讨鼠源重组UBC13蛋白对脂多糖(lipopolysaccharide,LPS)诱导的小鼠急性炎症的影响。将24只SPF雌性小鼠随机分成4组:PBS组,LPS模型组,重组UBC13蛋白高、低剂量组(分别为100和25μg/只),每组6只。LPS模型组与各蛋白剂量组腹腔注射20 mg/kg LPS,PBS组腹腔注射等体积PBS;注射结束1 h后,各蛋白组按相应剂量背部皮下多点注射重组UBC13蛋白,PBS组与LPS模型组注射等体积PBS。给予蛋白24 h后处死小鼠。收集小鼠肺脏、脾脏、胸腺及肝脏组织,计算脏器指数,HE染色观察组织病理学变化,实时荧光定量PCR检测肺脏、脾脏、胸腺和肝脏中IL-1β、TNF-α、IL-6 mRNA的相对表达量,以及肺脏中iNOS mRNA的相对表达量,综合评价鼠源重组UBC13蛋白对LPS诱导小鼠急性炎症的影响。结果显示,与PBS组相比,LPS模型组小鼠肺脏、脾脏及肝脏指数均显著或极显著升高(P<0.05;P<0.01),且肺脏、脾脏和肝脏组织均出现病理变化。实时荧光定量PCR结果显示,与PBS组相比,LPS模型组肺脏、脾脏、胸腺和肝脏中IL-1β、TNF-α、IL-6 mRNA相对表达量均极显著升高(P<0.01),肺脏中iNOS mRNA相对表达量也极显著升高(P<0.01);与LPS模型组相比,UBC13蛋白高剂量组肺脏、脾脏和肝脏中病理变化明显改善,肺脏、肝脏、脾脏中IL-1β、TNF-α、IL-6及肺脏中iNOS mRNA表达量均极显著降低(P<0.01);胸腺中TNF-αmRNA表达量显著降低(P<0.05),IL-6 mRNA和IL-1β表达量极显著降低(P<0.01)。表明鼠源重组UBC13蛋白可下调炎性因子的表达,从而改善LPS诱导的小鼠急性炎症反应。  相似文献   

20.
对5例巴氏杆菌感染家兔的空肠与圆小囊肥大细胞(mast cell,MC)进行了组织化学与电镜的观察,发现在细菌感染导致的病变组织边缘、病变组织内血管附近结缔组织中及变性细胞周围组织的上皮下与黏膜下层都出现了大量甲苯胺蓝(Toluidine Blue,TB)阳性肥大细胞。电镜下,MC有的直接与变性细胞密切接触,有的则和血管内皮紧密相触,在此部位的血管内可见有淋巴细胞贴附填充。MC胞浆内充盈大量的特征性颗粒,有时这些颗粒向细胞表面突出形成边缘空隙,即形成所谓的脱颗粒管道,将颗粒内容物逐渐排除细胞外,遗留空腔。  相似文献   

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