alpha- 细辛脑注射液对哮喘患儿血清COX-2，IL-8 及IgE 水平的影响及其 临床疗效

目的：评价琢-细辛脑注射液辅助治疗对哮喘患儿血清中COX-2、IL-8、IgE 水平的影响及其临床疗效。方法：选取我院哮喘 患儿96 例,随机分为实验组和对照组,各48 例,对照组采用常规药物治疗,实验组在此基础上加用琢-细辛脑注射液,观察患儿的 临床症状并测量血清中COX-2、IL-8、IgE 含量的变化情况。结果：实验组有效率明显高于对照组,差异具有统计学意义（x2=5.352, P=0.0207）;实验组喘息、呼吸困难、胸闷、咳嗽及哮鸣音等临床症状的消失时间明显低于对照组,差异均具有统计学意义（P<0. 05）;实验组治疗后血清COX-2、IL-8 及IgE 因子含量显著低于对照组,差异均具有统计学意义（P<0.05）。结论：琢- 细辛脑注射液 辅助治疗哮喘的疗效显著,能够降低患儿血清COX-2、IL-8 及IgE水平。     

传输靶向COX-2 siRNA联合化疗药物对大鼠胃癌细胞生长

目的：通过动物实验探讨传输靶向COX-2 siRNA联合化疗药物对大鼠胃癌细胞生长的抑制作用。方法：24 只健康SD 大鼠 平分为三组,治疗组用COX-2-siRNA转染的胃癌SGC7901 细胞接种,同时进行环磷酰胺、丝裂霉素C 化疗治疗;阴性对照组,用 阴性对照siRNA 转染的胃癌SGC7901 细胞接种,同时进行环磷酰胺、丝裂霉素C 化疗治疗;对照组(n=8),用未经转染的胃癌 SGC7901 细胞接种,不进行化疗治疗;三组转染后都接种了裸鼠。结果：治疗组、阴性对照组及对照组胃癌细胞凋亡率分别为 （22.28± 0.12）%、（1.23± 0.17）%和（1.03± 0.14）%,治疗组与阴性对照组和对照组比较差异都有统计学意义(t=18.152,17.555, P<0.05)。治疗组的抑瘤率为76.7%,阴性对照组和对照组分别为12.8%和6.89%,治疗组的抑瘤率明显高于其他两组(x2=15. 211,13.899,P<0.05)。Western blotting检测结果显示治疗组的COX-2 蛋白表达含量得到了明显抑制。结论：传输靶向COX-2 siRNA和化疗药物的配合应用可有效抑制COX-2 蛋白的表达,从而抑制胃癌细胞的生长,从而起到更好的治疗效果。     

新辅助化疗与营养支持对老年结肠癌患者T 细胞，COX-2 及tM2-PK水平的影响

目的：探讨新辅助化疗与营养支持综合治疗对老年结肠癌患者血清肿瘤标记物水平、COX-2 及生活质量影响及临床意义。 方法：选取我科收治的老年结肠癌患者80 例,根据治疗方案不同分为对照组与试验组。对照组常规行结肠癌根治切除术,试验组 应用FOLFOX3 方案。比较两组患者血清肿瘤标记物CEA 及CA19-9 水平、COX-2 水平及CD4+、CD8+及tM2-PK 水平。结果：与 治疗前相比,治疗后试验组和对照组CEA 及CA19-9 水平降低（P<0.05),COX-2、tM2-PK 水平降低（P<0.05),CD4+及CD4+/CD8+ 水平降低（P<0.05),CD8+水平升高（P<0.05)。与对照组比较,试验组COX-2、tM2-PK 水平、CD4+、CD8+水平改善明显优于对照组, 差异具有统计学意义（P<0.05),而CEA 及CA19-9 水平组间比较,差异无统计学意义（P>0.05）。结论：新辅助化疗与营养支持综合 治疗可杀伤老年结肠癌患者全身不可见转移肿瘤细胞,控制病情,临床疗效理想。     

胃苏颗粒联合四联疗法对Hp阳性慢性萎缩性胃炎患者血清胃肠激素和胃黏膜COX-2、NF-κB表达的影响

摘要 目的：观察胃苏颗粒联合四联疗法对幽门螺杆菌（Hp）阳性慢性萎缩性胃炎（CAG）患者血清胃肠激素和胃黏膜氧化酶-2（COX-2）、核转录因子-κB（NF-κB）表达的影响。方法：选取2017年7月~2019年6月期间中国人民解放军总医院第二医学中心消化内科收治的Hp阳性CAG患者120例,根据信封抽签法将患者分为观察组（60例,胃苏颗粒联合四联疗法）、对照组（60例,四联疗法）,均治疗2周。观察两组疗效、Hp根除率、胃肠激素和胃黏膜COX-2、NF-κB表达,观察两组治疗方案的药物安全性。结果：观察组的临床总有效率和Hp根除率均高于对照组（P<0.05）。观察组治疗2周后胃泌素（GAS）、胃动素（MTL）水平低于对照组,胃泌素-17（G-17）水平高于对照组（P<0.05）。观察组治疗后3个月的胃黏膜COX-2、NF-κB表达低于对照组（P<0.05）。两组不良反应发生率对比无差异（P>0.05）。结论：Hp阳性CAG患者采用四联疗法联合胃苏颗粒治疗,可有效控制患者胃肠激素水平,降低胃黏膜COX-2、NF-κB表达,疗效确切,且不良反应发生风险较低。     

乌司他丁对COPD合并呼吸衰竭患者血清COX-2，PGE2及PLA2 的影响

目的：探讨乌司他丁对慢性阻塞性肺疾病合并呼吸衰竭患者血清环氧化酶2（cyclooxygenase-2,COX-2）,前列腺素E2 （prostaglandin E2,PGE2）及磷脂酶A2（phospholipase A2,PLA2）浓度的影响。方法：选取2014 年1 月至2015 年1 月我院收治的 80 例慢性阻塞性肺疾病患者,按照单盲法均分为实验组和对照组。对照组给予慢性阻塞性肺疾病常规对症治疗;实验组在对照组 常规对症治疗的基础上,给予乌司他丁治疗。检测治疗前后患者COX-2、PGE2 及PLA2 血清浓度。结果：两组COX-2、PGE2 及 PLA2 血清浓度,实验组治疗后均显著低于治疗前（P<0.05）;对照组治疗后均低于本组治疗前,（P<0.05）。实验组治疗前与对照组 无显著差异（P>0.05）;治疗后,实验组COX-2、PGE2、PLA2 血清浓度显著低于对照组,治疗后实验组肺功能FEV1、FVC均显著优 于对照组（P<0.05）。结论：乌司他丁治疗慢性阻塞性肺疾病合并呼衰患者能够显著降低其COX-2、PGE2 及PLA2 血清浓度,有效 改善患者炎症反应、细胞损伤及临床症状,为临床积极治疗慢性阻塞性肺疾病提供新的思路。     

阿托伐他汀对急性冠脉综合征患者血脂蛋白相关磷脂酶A2 的影响

目的：探究阿托伐他汀对急性冠脉综合征（Acute Coronary Syndrome,ACS）患者血脂蛋白相关磷脂酶A2 的影响。方法：选取 我院2013 年12 月到2014 年11 月收治的急性冠脉综合征患者50 例,随机分为两组,其中对照组给予常规药物治疗,实验组予 以阿托伐他汀治疗。观察并比较两组患者的临床疗效及血清Lp-PLA2水平的变化情况。结果：经药物干预后,血脂各项指标（TG、 TC、HDL-C、LDL-C）均显著下降,与治疗前相比,差异具有统计学意义（P＜ 0.05）,治疗后实验组与对照组相比,血脂各项指标下降 更为明显,差异具有统计学意义（P＜ 0.05）;治疗后两组患者的血清Lp-PLA2 水平与治疗前均显著下降,经统计学分析,差异具有 统计学意义（P<0.05）,治疗后与对照组相比,实验组下降更为显著,差异具有统计学意义（P<0.05）。结论：阿托伐他汀可以明显改 善ACS 患者的各临床症状,降低血脂及血清Lp-PLA2 水平,为治疗ACS 的首选方法。     

左氧氟沙星联合利福平对肺结核患者血清降钙素原, IL-15及INF-r水平的影响

目的：探讨左氧氟沙星联合利福平对肺结核患者血清降钙素原、IL-15 及INF-酌水平的影响。方法：选择我院收治的肺结核患 者72 例，随机分为对照组和实验组，每组各36 例，所有患者均给予利福平以及肝泰乐口服治疗，实验组在对照组基础上给予左 氧氟沙星治疗。观察并比较两组患者治疗前后血清TCP，IL-15及INF-r水平的变化情况以及临床效果。结果：与治疗前相比，两组 患者治疗后TCP，IL-15 及INF-r水平均下降，差异具有统计学意义（P<0.05）；与对照组相比，实验组患者治疗后TCP，IL-15 及 INF-r水平较低，差异具有统计学意义（P<0.05）；实验组患者治疗总有效率（97.22%）高于对照组（86.11%），差异具有统计学意义 （P<0.05）。结论：左氧氟沙星联合利福平能够降低肺结核患者TCP、IL-15、INF-r水平，提高临床疗效，对临床有指导意义。     

乙肝病毒感染与B 细胞型非霍奇金淋巴瘤的相关性研究

目的：探讨乙肝病毒（HepatitisB virus, HBV）感染与B细胞型非霍奇金淋巴瘤（B-cell Non-Hodgkin''s Lymphoma,B-cell NHL） 的相关性。方法：回顾性分析2008 年1 月至2014 年1 月我院232 例NHL患者作为研究组,另选取经病理学、影像学等诊断为其 他类型肿瘤的患者230 例作为对照组。比较两组研究对象HAV、HBV及HCV 的感染情况。结果：研究组患者HBsAg阳性率高于 对照组,差异具有统计学意义（P<0.05）;但两组患者Anti-HAV和Anti-HCV 阳性率无明显差异（P>0.05）。B-cell NHL患者HBsAg 阳性率高于对照组和T-cell NHL患者,差异具有统计学意义（P<0.05）。T-cell NHL患者HBsAg阳性率与对照组无显著差异（P>0. 05）。B-cell NHL 年轻患者HBsAg 阳性率高于T-cell NHL患者,差异具有统计学意义（P<0.05）。B-cell NHL 患者Anti-HBs、 HBeAg、Anti-HBe及Anti-HBc阳性率与对照组存在明显差异（P<0.05）;而T-cellNHL患者与对照组无显著差异（P>0.05）。结论：B-cell NHL感染HBV 的几率较高,HBV 感染与B-cell NHL早期发病有明显的关联性。     

传输靶向COX-2 siRNA联合化疗药物对大鼠胃癌细胞生长的抑制作用

目的：通过动物实验探讨传输靶向COX-2siRNA联合化疗药物对大鼠胃癌细胞生长的抑制作用。方法：24只健康SD大鼠平分为三组,治疗组用COX-2-siRNA转染的胃癌SGC7901细胞接种,同时进行环磷酰胺、丝裂霉素C化疗治疗;阴性对照组,用阴性对照siRNA转染的胃癌SGC7901细胞接种,同时进行环磷酰胺、丝裂霉素C化疗治疗;对照组（n=8）,用未经转染的胃癌SGC7901细胞接种,不进行化疗治疗;三组转染后都接种了裸鼠。结果：治疗组、阴性对照组及对照组胃癌细胞凋亡率分别为（22．28±0．12）％、（1．23±0．17）％和（1．03±0．14）％,治疗组与阴性对照组和对照组比较差异都有统计学意义（t=18．152,17．555,P〈0．05）。治疗组的抑瘤率为76．7％,阴性对照组和对照组分别为12．8％和6．89％,治疗组的抑瘤率明显高于其他两组（x^2=15．211,13．899,P〈0．05）。Western blotting检测结果显示治疗组的COX-2蛋白表达含量得到了明显抑制。结论：传输靶向COX-2 siRNA和化疗药物的配合应用可有效抑制COX-2蛋白的表达,从而抑制胃癌细胞的生长,从而起到更好的治疗效果。     

慢性牙周炎患者龈沟液中IL-8 和TNF-alpha水平变化及临床意义

目的：探讨慢性牙周炎患者龈沟液中白细胞介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）水平变化及临床意义,为临床诊疗提 供参考。方法：选择2013 年12 月到2015 年12 月我院收治的60 例慢性牙周炎患者为实验组,选择同期60 例牙周健康者为对照 组。对照组对象于体检时、实验组患者于牙周常规治疗前后收集龈沟液并记录牙龈指数（GI）、牙龈沟出血指数（SBI）、菌斑指数 （PLI）、牙周袋探诊深度（PD）、临床附着丧失（CAL）等牙周临床指标。测量并比较两组对象龈沟液中IL-8 和TNF-α水平。结果：实 验组患者治疗前GI、SBI、PLI、PD 及CAL 等牙周临床指标均明显高于对照组,差异具有统计学意义（P<0.05）;治疗后,实验组患 者各牙周临床指标明显低于治疗前,差异有统计学意义（P<0.05）,但与对照组比较差异无统计学意义（P>0.05）。实验组患者治疗 前龈沟液中IL-8 和TNF-α水平均明显高于对照组,差异有统计学意义（P<0.05）;治疗后,实验组患者龈沟液中IL-8 和TNF-alpha水 平均明显低于治疗前,差异有统计学意义（P<0.05）。实验组患者治疗前龈沟液中IL-8 水平与牙周临床指标PD 呈正相关性（r=0. 495,P=0.027）,TNF-α水平与牙周临床指标SBI、PD 呈正相关性（r=0.512,0.673;P=0.019,0.012）。结论：慢性牙周炎患者龈沟液中 IL-8 和TNF-α具有较高水平,两者可能与慢性牙周炎的发生发展有关,对于临床诊断慢性牙周炎具有积极的临床意义。     

选择性co x 一2 抑制剂在胶质瘤放疗中的研究进展

环氧合酶（cyclooxygenase,COX）又名前列腺素内过氧化物合成酶,是前列腺素类似物合成的限速酶。COX-2是其诱导型酶。胶质瘤中COX-2的高表达被认为与肿瘤的侵袭性、预后相关。COX-2在胶质瘤的发生发展过程中发挥重要作用。选择性COX-2抑制剂通过直接和间接的作用机制而成为放射增敏剂。它们通过直接作用肿瘤细胞增强放射反应性,同时间接通过前列腺素影响肿瘤的血管形成抑制肿瘤生长。在体内和体外的研究表明选择性COX-2抑制剂可以增强胶质瘤对放射的反应性．降低恶性胶质瘤患者术后放射的必需照射剂量。而且在提高肿瘤放射敏感性的同时不增加对正常组织的放射损伤,甚至对正常组织有放射保护作用。因此,放疗联合选择性COX-2抑制剂可能成为胶质瘤治疗的新的有效途径。     

成釉细胞中COX-2的表达与影像学分型的关系

目的:探讨成釉细胞瘤中COX-2的表达和临床意义,以及COX-2的表达与成釉细胞瘤影像学分型之间的关系.方法:采用免疫组化S-P法检测60例成釉细胞瘤和22例正常口腔粘膜中COX-2蛋白的表达,同时收集相对应的60例成釉细胞瘤患者的手术前X线片并分型,结合COX-2蛋白在成釉细胞瘤中表达的结果进行分析.结果:60例成釉细胞瘤中COX-2的阳性表达率为80%(48/60),22例正常口腔粘膜中survivin表达率为36.36%(8/22),二者间差异有统计学意义(P<0.05).COX-2蛋白在患者的性别、发病部位及不同年龄组中的过表达率差异均无统计学意义(P>0.05).单房型成釉细胞瘤中COX-2的表达率较多房型和蜂窝型成釉细胞瘤低(P<0.05),多房型成釉细胞瘤和蜂窝型成釉细胞瘤中COX-2的表达率无差异(P>0.05).结论:COX-2可作为成釉细胞瘤诊断的一项重要指标;多房型和蜂窝型成釉细胞瘤的细胞增殖及侵袭能力较单房型高,多房型和蜂窝型成釉细胞瘤的手术方式不宜保守.     

COX-1/COX-2 inhibition assays and histopathological study of the new designed anti-inflammatory agent with a pyrazolopyrimidine core

Four pyrazolopyrimidine series were prepared with a substitution at position- 4 by Schiff base, triazole, oxadiazole and pyrazole moieties (7a-f, 8a,b, 9a-f, 10a,b and 13a,b), respectively. All the synthesized compounds were evaluated in vitro against COX-2 and in vivo against carrageenan-induced rat paw edema as anti-inflammatory agents. Regarding the anti-inflammatory activity (AI) compounds 7c, 7f, 8a, and 9a showed higher activity with respect to celecoxib. Compounds 9a, 7d, and 7f were closely selective to celecoxib. Also, 7c and 7d were safer than indomethacin and similar to celecoxib as resulted from the histopathological study. In addition, the docking study that showed the binding mode of prominent pyrazolopyrimidine compounds inside the COX-2 receptor. Formation of unexpected pyrazole 13a and 13b was briefly discussed using 2D NMR.     

Cox-2和Suvrivin蛋白在眼睑基底细胞癌组织中的表达

目的探讨Cox-2和Suvrivin蛋白在眼睑基底细胞癌组织中的表达及临床意义。方法收集武汉大学人民医院和武汉大学中南医院病理科1999-2006年手术切除及活检的眼睑基底细胞癌（basal cell carcinoma,BCC）标本共40例,另取癌周围组织5例作对照。眼睑基底细胞癌发病年龄20-68岁。采用免疫组织化学方法观察各组细胞内Cox-2和Suvrivin蛋白表达的变化。利用HPIAS-2000图像分析系统测定Cox-2和Suvrivin蛋白在以上各组中表达的平均光密度和平均阳性面积率。结果眼睑基底细胞癌组织中COX-2蛋白呈高表达;癌旁组织中COX-2蛋白呈低表达。眼睑基底细胞癌组织中Suvrivin蛋白呈高表达;癌旁组织中Suvrivin蛋白呈低表达。图像分析结果显示：眼睑基底细胞癌组织与癌旁组织之间COX-2和Suvrivin蛋白的平均光密度及阳性面积率的差异有显著性意义（P〈0.01）。结论COX-2、Survivin在眼睑BCC中的异常表达,对眼睑BCC的发生和发展起了重要作用。     

Toward the understanding of the molecular basis for the inhibition of COX-1 and COX-2 by phenolic compounds present in Uruguayan propolis and grape pomace

Propolis and grape pomace have significant amounts of phenols which can take part in anti-inflammatory mechanisms. As the cyclooxygenases 1 and 2 (COX-1 and COX-2) are involved in said mechanisms, the possibility for a selective inhibition of COX-2 was analyzed in vitro and in silico. Propolis and grape pomace from Uruguayan species were collected, extracted in hydroalcoholic mixture and analyzed. Based on phenols previously identified, and taking as reference the crystallographic structures of COX-1 and COX-2 in complex with the commercial drug Celecoxib, a molecular docking procedure was devised to adjust 123 phenolic molecular models at the enzyme-binding sites. The most important results of this work are that the extracts have an overall inhibition activity very similar in COX-1 and COX-2, i.e. they do not possess selective inhibition activity for COX-2. Nevertheless, 10 compounds of the phenolic database turned out to be more selective and 94 phenols resulted with similar selectivity than Celecoxib, an outcome that accounts for the overall experimental inhibition measures. Binding site environment observations showed increased polarity in COX-2 as compared with COX-1, suggesting that polarity is the key for selectivity. Accordingly, the screening of molecular contacts pointed to the residues: Arg106, Gln178, Leu338, Ser339, Tyr341, Tyr371, Arg499, Ala502, Val509, and Ser516, which would explain, at the atomic level, the anti-inflammatory effect of the phenolic compounds. Among them, Gln178 and Arg499 appear to be essential for the selective inhibition of COX-2.     

Mechanotransduction in bone cells proceeds via activation of COX-2, but not COX-1

Cyclooxygenase (COX) is the key enzyme in the production of prostaglandins, which are essential for the response of bone to mechanical loading. We determined which COX-isoform, COX-1 or COX-2, determines loading-induced prostaglandin production in primary bone cells in vitro. Mouse and human bone cells reacted to 1 h of pulsating fluid flow (PFF, 0.6+/-0.3 Pa at 5 Hz) with an increased prostaglandin E(2) production, which continued 24 h after cessation of PFF. Inhibition of COX-2 activity with NS-398 abolished the stimulating effect of PFF both at 1 h and at 24 h post-incubation, while inhibition of COX-1 by SC-560 affected neither the early nor the late response to flow. PFF rapidly stimulated COX-2 mRNA expression at 1 h but did not affect COX-1 mRNA expression. COX-2 mRNA expression was still significantly enhanced 24 h after cessation of PFF. We conclude that COX-2 is the mechanosensitive form of COX that determines the response of bone tissue to mechanical loading.     

Aromatase and COX-2 expression in human breast cancers

We have investigated aromatase and the inducible cyclooxygenase COX-2 expression using immunocytochemistry in tumors of a series of patients with advanced breast cancer treated with aromatase inhibitors. Aromatase was expressed in 58/102 breast cancers. This is similar to the percentage previously reported for aromatase activity. Interestingly, aromatase was expressed in a variety of cell types, including tumor, stromal, adipose, and endothelial cells. Since prostaglandin E₂ is known to regulate aromatase gene expression and is the product of COX-2, an enzyme frequently overexpressed in tumors, immunocytochemistry was performed on the tissue sections using a polyclonal antibody to COX-2. Aromatase was strongly correlated (P<0.001) with COX-2 expression. These results suggest that PGE₂ produced by COX-2 in the tumor may be important in stimulating estrogen synthesis in the tumor and surrounding tissue. No correlation was observed between aromatase or COX-2 expression and the response of the patients to aromatase inhibitor treatment. However, only 13 patients responded. Nine of these patients were aromatase positive. Although similar to responses in other studies, this low response rate to second line treatment suggests that tumors of most patients were no longer sensitive to the effects of estrogen. Recent clinical studies suggest that greater responses occur when aromatase inhibitors are used as first line treatment. In the intratumoral aromatase mouse model, expression of aromatase in tumors is highly correlated with increased tumor growth. First line treatment with letrozole was effective in all animals treated and was more effective than tamoxifen in suppressing tumor growth. Letrozole was also effective in tumors failing to respond to tamoxifen, consistent with clinical findings. In addition, the duration of response was significantly longer with the aromatase inhibitor than with tamoxifen, suggesting that aromatase inhibitors may offer better control of tumor growth than this antiestrogen.     

COX-1/COX-2 inhibition activities and molecular docking study of newly designed and synthesized pyrrolo[3,4-c]pyrrole Mannich bases

In the present paper we describe the biological activity of newly designed and synthesized series of pyrrolo[3,4-c]pyrrole Mannich bases (7a-n). The Mannich bases were obtained in good yields by one-pot, three-component condensation of pyrrolo[3,4–c]pyrrole scaffold (6a-c) with secondary amines and an excess of formaldehyde solution in C₂H₅OH. The chemical structures of the compounds were characterized by ¹H NMR, ¹³C NMR, FT-IR, and elemental analysis. Moreover, single crystal X-ray diffraction has been recorded for compound 7l. All synthesized derivatives were investigated for their potencies to inhibit COX-1 and COX-2 enzymes by colorimetric inhibitor screening assay. In order to analyse the intermolecular interactions between the ligands and cyclooxygenase, experimental data were supported with the results of molecular docking simulations. According to the results, all of the tested compounds inhibited the activity of COX-1 and COX-2.     

COX-2 regulates the proliferation of glioma stem like cells

Cancer stem-like cells (CSCs) possessing features of neural precursor cells (NPC) influence initiation, recurrence and chemoresistance of glioblastoma multiforme (GBM). As inflammation is crucial for glioblastoma progression we investigated the effect of chronic IL-1β treatment on CSCs derived from glioblastoma cell line U87MG. Exposure to IL-1β for 10 days increased (i) accumulation of 8-OHdG - a key biomarker of oxidative DNA damage; (ii) DNA damage response (DDR) indicators γH2AX, ATM and DNA-PK; (iii) nuclear and cytoplasmic p53 and COX-2 levels and (iv) interaction between COX-2 and p53. Despite upregulating p53 expression IL-1β had no effect on cell cycle progression, apoptosis or self renewal capacity of CSCs. COX-2 inhibitor Celecoxib reduced self renewal capacity and increased apoptosis of both control and IL-1β treated CSCs. Therefore the ability of COX-2 to regulate proliferation of CSCs irrespective of exposure to IL-1β, warrants further investigation of COX-2 as a potential anti-glioma target.     

COX-2和IL-1在甲状腺乳头状癌组织中的表达

目的探讨COX-2和IL-1在甲状腺乳头状癌组织中的表达及其在肿瘤的发生和发展中的作用。方法收集武汉大学人民医院和武汉大学中南医院病理科2000-2006年手术切除及活检的甲状腺乳头状癌标本共40例,另取癌周围组织5例作对照。采用免疫组织化学方法观察各组组织内COX-2和IL-1的表达。利用HPIAS-2000图像分析系统测定COX-2和IL-1在癌及癌旁组中表达的平均光密度和平均阳性面积率。结果甲状腺乳头状癌组织中COX-2和IL-1呈高表达;癌旁组织中COX-2和IL-1呈低表达。图像分析结果显示两组间差异有显著性意义（P〈0.01）。结论IL-1可能通过诱导COX-2的表达,在促进肿瘤的发生和发展中起作用。