[目的]探讨大肠腺癌组织中环氧合酶-2（COX-2）和组织蛋白酶D的表达及意义。[方法]采用免疫组织化学法检测62例大肠粘液腺癌标本及31例癌旁正常黏膜组织中COX-2和组织蛋白酶D的表达，分析其临床意义。[结果]大肠腺癌组织中COX-2和组织蛋白酶D的表达率分别为75．8％和82．3％，显著高于正常黏膜中的12．9％和22．6％，其差异有统计学意义（ P ＜0．01）；COX-2和组织蛋白酶D阳性表达与肿瘤大小及分化程度无关（ P ＞0．05），与浸润深度、淋巴结转移、Dukes分期呈正相关。[结论]在大肠癌恶变进程中，COX-2和组织蛋白酶D表达发生相应变化，其可能参与了大肠癌发生、发展的过程，两者联合检测可为临床判断大肠腺癌的恶性生物学行为提供参考。

[Objective] To explore the expression of cyclooxygenase-2(COX-2) and cathepsin D in large in-testinal adenocarcinoma and their significance .[Methods]immunohistochemical method was used to detect the expression of COX-2 and cathepsin D in 62 specimens of large intestinal mucinous adenocarcinoma and 31 nor-mal mucous tissue adjacent to the cancer .Clinical significance was analyzed .[Results]The expression rates of COX-2 and cathepsin D in large intestinal adenocarcinoma were 75 .8% and 82 .3% respectively ,which were markedly higher than those in normal mucosa(12 .9% and 22 .6% ) ,and there was significant difference( P 0 .05) ,but positively correlated with the depth of invasion ,lymph node metastasis and Dukes staging .[Conclusion] The expression of COX-2 and cathepsin D has the corresponding changes in the progression of large intestinal canceration ,which may participate in the occurrence and development of colon cancer .The de-tection of COX-2 combined with cathepsin D can provide

背景：有研究表明，基质金属蛋白酶所参与的细胞外基质降解在角膜新生血管形成过程中起关键作用，组织因子途径抑制物2是新近发现的一种新型的丝氨酸蛋白酶抑制物，能有效抑制基质金属蛋白酶的活性。 目的：观察组织因子途径抑制物2对体外角膜基质细胞表达基质金属蛋白酶活性的关系。 方法：在体外对兔角膜基质细胞进行原代及传代培养，用脂质体介导的人类组织因子途径抑制物2真核表达载体转染兔角膜基质细胞，G418筛选阳性细胞。 结果与结论：RT-PCR，Western blot及明胶酶谱法分析结果显示，转染后角膜基质细胞组织因子途径抑制物2 mRNA和蛋白质的表达均上调(P<0.05)，而基质金属蛋白酶1，2的活性下降(P<0.05)。结果提示，组织因子途径抑制物2可明显抑制角膜基质细胞中基质金属蛋白酶1，2的活性。

BACKGROUND:The degradation of extracellular matrix, which is mediated by matrix metal oproteinases, plays a crucial role in the corneal neovascularization. Tissue factor pathway inhibitor 2, a new type serine proteinase inhibitor, can effectively inhibit the activity of matrix metal oproteinases. OBJECTIVE:To elucidate the effect of tissue factor pathway inhibitor 2 on the expressions of matrix metal oproteinases in keratocytes in vitro. METHODS:Rabbit keratocytes were primarily cultured and subcultured in vitro. Plasmid vector pBos-Cite-neo/TFPI-2 was transfected into keratocytes with Lipofectamine 2000. The positive cells were selected using G418. RESULTS AND CONCLUSION:The results of reverse transcription-polymerase chain reaction, western blot analysis and gelatinase zymography analysis showed that, expression of mRNA and protein of tissue factor pathway inhibitor 2 was upregulated in the transfected keratocytes (P<0.05), while activity of matrix metal oproteinase 1 and 2 was signi

基质金属蛋白酶是一组金属依赖的可降解细胞外基质的蛋白酶类.基质金属蛋白酶与基质金属蛋白酶组织抑制因子之间的比例失衡可能导致细胞外基质的降解异常,这可以促进纤维化的过程.近年来随着研究的进展,发现基质金属蛋白酶-2和基质金属蛋白酶-9与特发性肺纤维化有着密切的关系,现就此作一综述.

Matrix metalloproteinase (MMPs) is a kind of protease with metals dependence which can degrade extracellular matrix.Imbalance in MMPs and tissue inhibitor of matrix metalloproteinase may lead to abnormal degration of extracellular matrix.Previous research has indicated that MMP-2 and MMP 9 have a close relationship with idopathic pulmonary fibrosis.This article reviews the relationship of MMP 2.MMP-9 with idopathic pulmonary fibrosis.

目的探讨糜蛋白酶在烟草烟雾所诱导的肺动脉重构和肺动脉高压中的作用。方法将仓鼠暴露在烟草产生的烟雾中（烟雾暴露组,n=6）,4个月后,使用免疫组织化学法、蛋白免疫印迹法、放射免疫学测定、反转录PCR等测定仓鼠肺的形态学和肺组织的生物化学改变。对烟雾暴露组与对照组（n=6）上述指标进行比较。结果长期烟草烟雾暴露使仓鼠右心室收缩压升高,肺小动脉中层细胞肥大,同时肺组织糜蛋白酶活性及合成增加,血管紧张素Ⅱ（AngⅡ）水平升高（与对照组比较,P均﹤0.05）。糜蛋白酶抑素（chymostatin）可以降低烟草诱导的仓鼠肺组织中糜蛋白酶活性的增加和AngⅡ水平,改善肺小动脉的重构程度,降低右心室收缩压,但对仓鼠肺组织中血管紧张素转换酶（ACE）的活性无影响。结论长期烟草烟雾暴露可增加仓鼠肺中糜蛋白酶的活性及表达,激活的糜蛋白酶进一步诱导肺组织AngⅡ形成,这可能是烟草诱导的肺动脉高压发生机制的一部分。因此,糜蛋白酶抑素也许会对吸烟的肺动脉高压患者有益。

Objective The aim of this study was to determine the potential role of chymase in ciga-rette smoke-induced pulmonary arterial remodeling and hypertension.Methods Hamsters were exposed to cig-arette smoke for 4 months (smoke-exposed group,n =6).After smoke exposure,lung morphology and tissue biochemical changes were examined using immunohistochemistry,Western blotting,radioimmunoassay and re-versetranscription polymerase chain reaction.Comparison of these indicators in the smoke-exposed group and the control group (n =6).Results Chronic exposure to cigarette smoke significantly induced elevation of right ventricular systolic pressures and medial cells hypertrophy of pulmonary arterioles in hamsters,concurrent with an increase in the activity and synthesis of chymase in the lung.Elevated Ang Ⅱ levels was also observed in smoke-exposed lungs (compared with the control group,all P <0.05).Chymostatin could reduce the ciga-rette smoke-induced increase in chymase activity and Ang

COPD 是一种以气流受限为特征,并伴有肺功能进行性降低的异常炎症反应相关的疾病。其主要原因是细胞外基质在气道壁过度沉积,引起气道阻塞和肺弹性基质的降解。COPD 的发生中,气道炎症、氧化/抗氧化失衡、蛋白酶/抗蛋白酶失衡起着重要的作用。其中,α1-抗胰蛋白酶(α1-antitrypsin,α1-AT)缺乏症与 COPD 有着重要联系,本文主要就目前对于蛋白酶/抗蛋白酶系统中起主要作用的中性粒细胞弹性蛋白酶/α1-AT、基质金属蛋白酶/基质金属蛋白酶组织抑制物的结构、功能、诊断与治疗作一综述。

Chronic obstructive pulmonary disease (COPD)is an abnormal inflammatory reaction related disease,characterized by airflow limitation and accompanied by progressive lowering lung function. The etiology is the excessive deposition of extracellular matrix in the wall of airway,leading to airway obstruction and degradation of elastic matrix in lung.Airway inflammation,oxidation/antioxidation disequilibrium and protease/antiprotease imbalance play critical roles during the development of COPD. Among them,α1-antitrypsin (α1-AT)deficiency has an important connection to COPD.The present article is committed to review on the current progress of the structure,function,diagnosis and treatment of neutrophil elastase/α1-AT (NE/α1-AT ) and matrix metalloproteinase/tissue inhibitor of metalloproteinase (MMPs/TIMP)in the protease/antiprotease system.