COX-2、VEGF以及MVD在子宫内膜异位症中的表达及意义

目的通过探讨环氧合酶-2（COX-2）、血管内皮生长因子（VEGF）以及微血管密度（MVD）在子宫内膜异位症（EMs）在位内膜、异位内膜及正常子宫内膜组织中的表达,探讨子宫内膜异位症的发病机制。方法采用免疫组化SP法检测EMs患者32例在位内膜、28例异位内膜及40例对照组正常子宫内膜中COX-2、VEGF的蛋白表达,计数微血管密度（MVD）值,并进行相关性分析。结果 （1）COX-2、VEGF在EMs在位内膜、异位内膜阳性表达率明显高于正常对照组,差异具有统计学意义（P〈0.05）,EMs异位内膜组COX-2、VEGF阳性表达率高于在位内膜组,差异有统计学意义（P〈0.05）。（2）MVD的计数在正常对照组,在位内膜组,异位内膜组依次递增,在位内膜组、异位内膜组与正常对照组比较有统计学差异（P〈0.05）,而在位内膜组与异位内膜组比较有统计学差异（P〈0.05）。（3）EMs在位内膜、异位内膜组患者和正常对照组COX-2蛋白表达与VEGF蛋白及MVD值的变化呈正相关。结论 COX-2与VEGF在EMs中的高表达,与子宫内膜异位的血管生成有关。     

眼缺血再灌注损伤大鼠葡萄膜组织COX-2的表达及意义

目的:探讨实验大鼠眼缺血再灌注后葡萄膜组织中环氧合酶-2(COX-2)的表达及意义。方法:通过血管结扎法建立大鼠一侧眼缺血再灌注损伤模型,并以对侧眼作为假手术对照,检测实验眼分别缺血1h、2h、3h、4h、5h、6h情况下,脉络膜和虹膜组织中COX-2和血管内皮生长因子(VEGF)的表达。结果:在各组实验眼脉络膜和虹膜各层组织中都有不同程度COX-2和VEGF阳性表达,与假手术对照眼比较有显著性差异,P<0.01;且脉络膜或虹膜中COX-2和VEGF表达具有良好相关性,分别为r=0.943,r=0.886。结论:与炎症密切相关的COX-2可能作为潜在的血管增生刺激因子,在葡萄膜新生血管形成中起着重要作用。     

食管癌COX-2和VEGF的表达及其与临床病理特征的关系

目的探讨COX-2、VEGF在食管癌组织中的表达及其与食管癌临床病理特征的相关性及两者关系。方法免疫组化方法检测68例手术切除的食管癌组织中COX-2、VEGF的表达,分析两者表达与食管癌临床病理特征的相关性及两者关系。结果 COX2和VEGF在正常食管组织中未见表达或很少表达,而在食管癌组织中COX-2阳性率79.4%;VEGF-C阳性率72.1%。食管癌的分化程度越低,COX-2的表达越高,两者有明显相关性,P〈0.05;但VEGF的表达与分化程度无明显相关性,P〉0.05。COX-2、VEGF的表达均随浸润深度增加而逐渐增加,两者均呈正相关,P〈0.05;两者在无淋巴结转移的食管癌组织中的表达均明显低于有淋巴结转移及远处转移者（P〈0.01）,两者呈正相关。同样,COX-2、VEGF的表达与TNM分期相关。结论 COX-2、VEGF在食管癌中呈高表达状态,并且这种高表达与食管癌的病理特征包括分化程度、浸润深度、淋巴结转移及TNM分期相关,COX-2与VEGF的表达与食管癌的浸润深度、淋巴结转移及TNM分期的关系呈正相关。     

实验性脑出血大鼠出血灶周组织环氧合酶-2的表达

目的 探讨实验性大鼠腩出血后出血灶周脑组织环氧合酶-2(COX-2)的表达及其意义.方法 采用自体注血法制作脑出血模型,免疫组织化学染色检测脑出血后不同时间点出血灶周组织COX-2表达.结果 正常对照组及出血对侧组脑组织几乎无COX-2表达,在脑出血灶周的脑组织可见COX-2阳性细胞,COX-2阳性细胞数于出血后3 h开始增多,出血48 h达高峰.结论 脑出血后早期血肿灶周组织COX-2表达随出m时间延长而增高.     

COX-2和VEGF在人脑星形细胞瘤中的表达及与临床病理分级的相关性

目的探讨环氧化酶-2(COX-2)和血管内皮生长因子(VEGF)在人脑星形细胞瘤中的表达及其与肿瘤临床病理分级的关系。方法通过免疫组化SP法测定COX-2和VEGF在50例人脑星形细胞瘤和10例正常脑组织中的表达。结果COX-2、VEGF在人脑星形细胞瘤中的表达高于正常脑组织(P<0.001)。COX-2和VEGF与人脑星形细胞瘤临床病理分级显著相关(P<0.05)。人脑星形细胞瘤中COX-2与VEGF的表达存在相关性。结论COX-2和VEGF参与人脑星形细胞瘤的发生、发展且与其恶性表型有关;COX-2可能与人脑星形细胞瘤的血管形成有关。     

人脑胶质瘤中COX-2表达及其与血管新生关系

目的 检测COX-2、VEGF和CD34在人脑胶质瘤中的表达,探讨COX-2、VEGF与胶质瘤微血管密度及血管新生之间的关系及意义.方法 用免疫组化SP法检测80例胶质瘤及10例正常脑组织中COX-2、VEGF和CD34的表达.结果COX-2与VEGF阳性细胞在坏死区周围及血管密集的区域分布密集,80例胶质瘤中二者表达的阳性率分别为68.8%和72.5%,正常脑组织中无表达;COX-2、VEGF的表达与MVD之间成正相关(r=0.927,r=0.939,P<0.05),COX-2与VEGF的表达成正相关(r=0.885,P<0.05),胶质瘤病理级别与COX-2、VEGF、MVD之间均成正相关(r=0.894,r=0.927,r=0.865,P<0.05).结论 COX-2和VEGF在胶质瘤的生长和进展过程中发挥重要作用,与其恶性度关系密切;COX-2可能通过上调VEGF的表达促进肿瘤组织血管新生.     

口虾蛄提取物对人鼻咽癌细胞P53、COX-2和VEGF表达的影响

目的: 研究口虾蛄提取物(EOS)对人低分化鼻咽癌细胞系(CNE-2Z)中P53、环氧化酶2(COX-2)和血管内皮生长因子(VEGF)表达的影响及意义。方法: 不同浓度EOS(0 mg/L、125 mg/L、250 mg/L和500 mg/L)作用CNE-2Z细胞24 h后,Western blotting检测P53蛋白表达,免疫细胞化学法及RT-PCR法分别检测COX-2 、VEGF蛋白和mRNA的表达。结果: CNE-2Z细胞中P53蛋白、COX-2和VEGF蛋白和mRNA表达均随EOS作用浓度增高而逐渐降低,呈量效关系(P<0.01);且COX-2 和VEGF表达量呈正相关(P<0.05),COX-2 和P53表达量亦呈正相关(P<0.05)。结论: EOS可能通过抑制CNE-2Z细胞中P53蛋白的表达,干扰COX-2和VEGF的表达而发挥其抗肿瘤作用的。     

2型糖尿病患者血浆中COX-2与VEGF的变化及其与尿蛋白水平的相关性研究

目的通过检测糖尿病患者血浆中环氧化酶同工酶-2（COX-2）与血管内皮生长因子（VEGF）的变化,了解COX-2及VEGF水平的变化及其与患者尿蛋白定量之间的关系。方法收入51例2型糖尿病患者及47例年龄/性别匹配的健康志愿者,以ELISA法检测其血浆中COX-2与VEGF的水平,同时对研究对象的尿蛋白水平等肾功能指标进行检测,并对两组指标进行相关性分析。结果糖尿病患者血浆COX-2水平（55.58±8.84）ng/mL及VEGF水平（377.59±38.60）pg/mL均显著高于对照组[COX-2（0.89±0.27）ng/mL,VEGF（43.51±8.61）pg/mL]（P均〈0.01）;COX-2与VEGF之间存在正相关,差异有统计学意义（r=0.983,P〈0.01）,COX-2及VEGF与患者尿蛋白之间均存在正相关,差异有统计学意义（COX-2与尿蛋白r=0.728,P〈0.01;VEGF与尿蛋白r=0.769,P〈0.01）;COX-2及VEGF与患者血肌酐之间均存在正相关,差异有统计学意义（COX-2与血肌酐r=0.649,P〈0.01;VEGF与血肌酐r=0.619,P〈0.01）。结论2型糖尿病患者血浆中存在明显升高的COX-2及VEGF,并与患者尿蛋白水平及血肌酐水平存在相关性,提示COX-2及VEGF可能参与糖尿病肾病的发病过程。     

环氧合酶2抑制剂对肝肿瘤细胞的血管内皮生长因子表达的影响

目的探讨肝肿瘤细胞环氧合酶2(COX-2)和血管内皮生长因子(VEGF)关系。方法实验分为对照组和实验组,培养肝癌细胞株(BEL-7402)作为对照组,培养肝癌细胞株用不同浓度赛来昔布(celeccoxib商品名:西乐葆)处理作为实验组;提取mRNA,用ELISA方法检测细胞培养基中VEGF水平,用RT-PCR分别检测COX-2和VEGF的mRNA。结果正常培养的肝癌细胞能同时检测到COX-2和VEGF的mRNA;COX-2抑制剂赛来昔布能抑制VEGF的表达;COX-2在mRNA水平调控VEGF的表达。结论COX-2在VEGF的分泌与合成中起重要作用,从而影响肿瘤新生血管生成及肿瘤生长。     

胆囊癌中VEGF和MMP-2的表达及其相关性

目的研究VEGF和MMP-2的表达及其与胆囊癌临床生物学行为的关系。方法选取手术切除胆囊癌标本46例,采用免疫组化SP法检测VEGF、MMP-2蛋白的表达和平均血管密度(MVD)。结果胆囊癌VEGF阳性率54.3%,其VEGF的表达与肿瘤中MVD计数及胆囊癌的分化程度、浸润深度、淋巴结转移密切相关。胆囊癌MMP-2阳性率73.9%,MMP-2的表达与胆囊癌的淋巴结转移密切相关。MMP-2和VEGF在胆囊癌组织中的表达有一定的相关性。结论 MMP-2和VEGF在胆囊癌的血管形成及肿瘤进展、转移中起重要作用并相互协同促进,为临床使用抗血管治疗及基质金属蛋白酶抑制剂的治疗提供参考依据。     

Differential expression of COX-1 and COX-2 in the gastrointestinal tract of the rat

The aim of this study was to use immunohistochemistry with morphometry to investigate COX-1 and COX-2 expression in the normal rat gastrointestinal (GI) tract and examine if sites of ulceration previously observed with long-term COX-2 inhibitor administration in mice correlate with differential COX-1/COX-2 expression. COX-2 positive cells were observed predominantly in the apical lamina propria of intestinal villi with fewer cells in the mucosal epithelium. The highest level of COX-2 expression was observed at the ileocaecal junction (ICJ). COX-2 expression was also present in parasympathetic ganglia of the submucosa and muscularis. In the stomach, the highest grade of COX-2 expression was observed in the apical lamina propria of the fundus adjacent to the junctional ridge. In contrast, COX-1 positive cells within the lamina propria were evenly distributed along the GI tract but were present in higher numbers than COX-2 positive cells. The mean level of COX-1 expression at the ICJ was not significantly different from the ileum and caecum. Evidence that the highest level of COX-2 expression in normal rats is located on the ileal side of the ICJ provides the first mechanism to explain spontaneous ulceration and perforation of the distal ileum in COX-2 -/- animals.     

VEGF rs3025039和rs3025021多态性与胃癌组织中VEGF、COX-2表达的关系

目的研究血管内皮生长因子(VEGF)基因单核甘酸多态性与安徽地区胃癌易感性关系以及与胃癌临床病理特征和胃癌组织VEGF、环氧化酶-2(COX-2)蛋白表达的关系。方法采用基因测序仪对安徽地区238例胃癌患者及425例正常对照组血样进行VEGF rs3025039和rs3025021的多态性测序,用组织芯片技术及免疫组化法检测相应胃癌组织和30例癌旁组织中VEGF和COX-2的分布。结果与正常对照相比,胃癌患者VEGF rs3025039TT基因型可能增加胃癌风险性(P=0.047,OR=2.86,95%CI=1.01～8.08)。rs3025021CT基因型显著降低胃癌风险性(P=0.032,OR=0.65,95%CI=0.44～0.96)。胃癌组织VEGF和COX-2的阳性率分别为62.6%及61.8%,显著高于癌旁组织的26.7%(P=0.000)和36.7%(P=0.008),并与TNM分期、肿瘤大小、浸润深度、淋巴结转移、临床分期(仅VEGF)及组织学类型(仅COX-2)有关(P=0.001～0.05)。VEGF表达与COX-2呈正相关(rs=0.178,P=0.006)。除VEGF rs3025021与肿瘤大小有关(P=0.026)外,VEGF rs3025039和rs3025021与胃癌临床病理学参数及VEGF及COX-2表达均无关。结论VEGF rs3025039和rs3025021多态性影响安徽地区的胃癌易感性,对胃癌组织VEGF表达无明显影响;VEGF及COX-2表达与胃癌的肿瘤侵袭性密切相关,二者对胃癌的恶化进展可能有一定的协同作用。     

COX-2和VEGF在急性白血病患者体内表达

环氧化酶-2(COX-2)是花生四烯酸转化成前列腺素过程中的重要限速酶.研究表明其在多种实体瘤中表达增强,并认为其与肿瘤血管的生成、肿瘤的发生、浸润和转移密切相关,是肿瘤防治的新靶点.     

Induction of COX-2 expression by acrolein in the rat model of hemorrhagic cystitis

AIM: Acrolein (ACR) is a urinary metabolite of cyclophosphamide (CPS) and ifosfamide (IFS), which has been demonstrated to be the causative agent of hemorrhagic cystitis (HC), induced by these compounds. In this study, we investigate the participation of cyclooxygenase-2 (COX-2) on ACR-induced HC. METHODS: Male Wistar rats (150-200g; six rats per group) were treated with distilled water or intravesical ACR and analyzed by changes in bladder wet weight, macroscopic and microscopic parameters and COX-2 expression. RESULTS: COX-2 immunohistochemical expression was significant 12h after ACR administration mainly in subepithelial cells. ACR injection also alters some macroscopic and microscopic parameters in bladder of rats analyzed by Gray's criteria. CONCLUSIONS: COX-2 participates in the pathogenesis of ACR-induced HC first seen 12h after initial contact between ACR and urothelium.     

Correlation of E-cadherin, VEGF, COX-2 expression to prognostic parameters in papillary thyroid carcinoma

Thyroid cancer represents approximately 1% of all human malignancies. papillary thyroid carcinoma (PTC) is the most common malignant tumor of the thyroid gland, accounting for 70–80% of all thyroid cancers. In the US, the incidence of thyroid cancer is 4 per 100,000 individuals. It is two to four times as frequent in women as in men.The development of PTC is influenced by many factors including genetic alterations, growth factors, and physical agents such as radiation.In order to recognize the prognosis for PTC, a lot of clinic and pathological parameters such as; age, tumor size, extra-thyroid tumor spread, lymph node, distant metastases, gender, tumor stage are used. As most of these parameters are subjective, more objective and useful prognostic factors are needed for determining biologic behavior, providing an initial assessment.In this study, we aimed to compare the expressions of COX-2, E-cadherin, VEGF to classical prognostic factors, and to investigate the correlation with prognosis. Operation records from 79 PTC cases were examined retrospectively. In the study, we aimed to investigate the whole tissue by means of stereology method, which is an impartial one, and we indicated the expression COX-2, VEGF, E-cadherin immunohistochemically in 79 resection diagnosed with PTC. We determined correlations between the expressions of COX-2 and VEGF, E-cadherin, and age, gender, and stage.     

Localization of COX-1 and COX-2 in the intracranial dura mater of the rat

Primary headaches such as migraine can be aborted by systemic administration of non-steroidal anti-inflammatory drugs (NSAIDs), potentially through the non-selective inhibition of cyclooxygenase (COX) activity in the intracranial meninges. In this study we have used single and double labeling immunohistochemistry to examine the distribution of the COX-1 and COX-2 isoforms in the intracranial dura mater of the rat and identify cell types that express them. COX-1 immunoreactivity was found in medium and small dural blood vessels and was co-expressed with the endothelial cell markers vimentin and the endothelial isoform of nitric oxide synthase (ecNOS). COX-1 was also found to be present in most dural mast cells. COX-2 was mainly expressed in ED2-positive resident dural macrophages. Constitutive COX-2 expression was also found in some axonal profiles, many of which were co-labeled with the nociceptor peptide marker CGRP. The findings suggest that NSAIDs may abort headache, at least in part, by inhibiting either neuronal or non-neuronal COX activity in the dura mater.     

COX-1 and COX-2 expression in feline oral squamous cell carcinoma

This study demonstrated immunohistochemically the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in feline oral squamous cell carcinoma (FOSCC), with primary polyclonal antibodies raised against human epitopes. COX-2 immunolabelling was intracytoplasmic and, in some neoplastic cells, perinuclear; it was demonstrated in a small proportion (< or = 1%) of neoplastic cells and its intensity was usually mild to moderate. In contrast, all neoplastic tissues showed extensive nuclear and cytoplasmic COX-1 immunolabelling. Cytoplasmic COX-1 immunolabelling was less intense than nuclear labelling in neoplastic tissue. In the adjacent histologically normal oral mucosa, COX-2 immunolabelling was absent. The cytoplasmic and nuclear intensity and distribution of COX-1 immunolabelling was significantly higher in neoplastic tissue than in adjacent normal oral mucosa. The results indicate that COX-1 and COX-2 are overexpressed in FOSCC, but the clinical and pathophysiological significance of this finding remains to be determined.     

Temporospatial patterns of COX-2 expression and pyramidal cell degeneration in the rat hippocampus after trimethyltin administration

The temporospatial profile of cyclooxygenase-2 (COX-2) expression and neuronal degeneration following trimethyltin (TMT) administration was investigated in the rat hippocampus region. In the CA1 region, significant COX-2 expression was detected on day 3 after TMT administration but pyramidal cell degeneration was detected only on day 5 and thereafter. In the CA3 region, on the other hand, the constitutive COX-2 expression remained unchanged, and more severe pyramidal cell degeneration started on day 3. Concomitant with these observations, we observed that the coadministration of a COX-2 inhibitor prevented such neuronal degeneration only in the CA1 region and not in the CA3 region. In addition, COX-2 inhibition did not affect the increase in the plasma corticosterone concentration after TMT administration. Furthermore, the COX-2 inhibitor did not alleviate TMT-induced locomotor hyperactivity in rats, for which inhibitors of corticosterone synthesis are known to be effective. These data suggest that the COX-2-dependent pathway appears to assist TMT-induced degeneration of CA1 pyramidal cells but not CA3 pyramidal cells in a corticosterone-independent manner.     

环氧合酶-2抑制剂对大鼠骨关节炎模型软骨中血管内皮生长因子表达的影响

目的研究环氧合酶-2抑制剂(吲哚美辛)对大鼠骨关节炎模型关节软骨中血管内皮生长因子(VEGF)表达的影响。方法健康雄性wistar大鼠30只,随机均分为对照组、骨性关节炎组(OA组)和吲哚美辛处理组。利用膝关节注射4%的木瓜蛋白酶溶液的方法制作骨关节炎模型。采用关节炎评分法评定各组大鼠平均关节炎指数(MAI),免疫组化方法与Western blot方法检测关节软骨中VEGF蛋白的表达变化。结果 OA模型组随着造模的时间延长,关节出现了重度红肿现象,对照组关节无任何异常变化;与OA模型组比较,吲哚美辛组的关节炎症反应呈现消退现象。VEGF蛋白在对照组大鼠关节软骨仅有微量表达,而在术后8周OA组大鼠关节软骨表达则显著升高(P0.01);与OA组相比,吲哚美辛组大鼠关节软骨中VEGF蛋白表达显著降低(P0.01)。结论吲哚美辛对骨关节炎的抑制作用可能与下调VEGF蛋白的表达相关。