清解扶正颗粒体外抑制血管新生的作用机制研究

目的:探讨清解扶正颗粒(Qingjiefuzheng Granules,QFG)对体外人脐静脉内皮细胞(Human Umbilical Vein Endothelial Cells,HUVEC)新生的影响及可能的作用机制。方法:以HUVEC为研究对象,给予不同浓度QFG后观察细胞形态变化,MTT检测细胞活力,划痕实验检测细胞迁移能力,管腔形成实验检测细胞成血管能力,蛋白免疫印迹检测促血管新生因子、血管内皮生长因子A、血管内皮生长因子受体2、基质金属蛋白酶2及基质金属蛋白酶9的蛋白表达。结果:QFG对HUVEC形态与细胞生长没有明显影响,但可显著抑制HUVEC的活力、迁移及体外成血管能力;QFG显著抑制血管内皮生长因子A、基质金属蛋白酶2、基质金属蛋白酶9等蛋白表达。结论:QFG在体外具有抑制血管新生的作用,其作用机制与其抑制血管内皮生长因子A、基质金属蛋白酶2及基质金属蛋白酶的表达有关。     

狗肝菜多糖对肝纤维化大鼠肝组织MMP-1及TIMP-1表达的影响

目的研究中药狗肝菜多糖对二甲基亚硝胺诱导的肝纤维化大鼠肝组织中基质金属蛋白酶-1(matrixmetalloproteinase-1,MMP-1)及基质金属蛋白酶抑制剂-1(tissueinhibitor of matrix metalloproteinase-1,TIMP-1)蛋白表达的影响。方法用二甲基亚硝胺诱导大鼠肝纤维化模型,不同浓度狗肝菜多糖干预后,取肝脏常规制片并HE染色,观察各组大鼠肝组织病理学改变,免疫组织化学方法检测各组大鼠肝组织MMP-1及TIMP-1蛋白表达的情况。结果狗肝菜多糖高、中剂量组中大鼠肝组织MMP-1蛋白表达较模型组明显升高(P<0.05),狗肝菜高、中剂量组中大鼠肝组织TIMP-1蛋白表达较模型组明显降低(P<0.05)。结论狗肝菜多糖具有显著的抗肝纤维化作用,其机制可能与提高MMP-1表达,降低TIMP-1蛋白的表达而调控细胞外基质的代谢有关。     

基质金属蛋白酶-9及血管内皮生长因子在卵巢癌中表达及其关系研究

目的:探讨基质金属蛋白酶-9及血管内皮生长因子与肿瘤侵袭发展的关系及二者相关性.方法:80例卵巢癌及30例卵巢良性肿瘤患者,采用RT-PCR和免疫组织化学方法检测基质金属蛋白酶-9及血管内皮生长因子的表达情况.结果:卵巢癌组基质金属蛋白酶-9及血管内皮生长因子mRNA的表达(1.128±0.061,0.878±0.034)明显高于卵巢良性肿瘤组(0.426±O.085,0.178±O.050)(P<0.05).卵巢癌组中基质金属蛋白酶-9与血管内皮生长因子蛋白的阳性表达(93.8%,97.5%)明显高于卵巢良性肿瘤组(43.3%,53.3%)(P<0.05),卵巢癌组中基质金属蛋白酶-9与血管内皮生长因子蛋白的表达与临床分期、有无淋巴结转移有关,二者阳性表达率成正相关(r=0.74,P<0.05).结论:基质金属蛋白酶-9及血管内皮生长因子高表达与卵巢癌侵袭性密切相关,可作为检测卵巢癌侵袭性的有效指标.在肿瘤侵袭过程中基质金属蛋白酶-9与血管内皮生长因子的产生关系密切.     

人胎盘天然金属蛋白酶抑制因子3的分离纯化

背景：基质金属蛋白酶是一类可促进肿瘤生长和转移的蛋白分解酶家族，其活性可被组织金属蛋白酶抑制因子所抑制。其中组织金属蛋白酶抑制因子3的抑制作用更为重要。 目的：旨在从人胎盘中完全分离纯化天然组织金属蛋白酶抑制因子3，并建立组织金属蛋白酶抑制因子3酶联免疫测定方法。 设计：单一样本观察。 单位：沈阳医学院中心实验室。 材料：人胎盘来自沈阳医学院附属奉天医院妇产科（家属知情同意）；基质金属蛋白酶l来自富士药品研究所。 方法：实验于2001-03／2002-05在沈阳医学院中心实验室完成。①利用4mol/L尿素Tris缓冲液（pH8．0），制备胎盘匀浆液。②匀浆液经CM52阳离子交换树脂层析和SephacrylS-200凝胶过滤二步柱层析。③SDS-聚丙烯酰胺凝胶电泳检测相对分子量及纯度。④Western blotting鉴定纯化蛋白的性质。⑤免疫荧光法测定组织金属蛋白酶抑制因子3对基质金属蛋白酶l的抑制率。 主要观寨指标：①聚丙烯酰胺电泳法所示蛋白带相对分子质量。②Western blot的显色结果。③组织金属蛋白酶抑制因子3对基质金属蛋白酶l的抑制率。④纯化后组织金属蛋白酶抑制因子3的回收率。 结果：①人胎盘分离纯化的组织金属蛋白酶抑制因子3分为非糖化和糖化两种，相对分子质量分别为24000和27000两种。②非糖化和糖化的组织金属蛋白酶抑制因子3对基质金属蛋白酶l的抑制活性分别为1.1&;#215;10^10mol／L和1．2&;#215;10^10mol／L。胎盘来源的组织金属蛋白酶抑制因子3对基质金属蛋白酶l的抑制活性明显高于重组的组织金属蛋白酶抑制因子3。③二步层析后组织金属蛋白酶抑制因子3的回收率为23．4％。 结论：人胎盘胞外基质来源的组织金属蛋白酶抑制因子3是由非糖基化蛋白和糖基化蛋白组成；两种纯化的组织金属蛋白酶抑制因子3对基质金属蛋白酶l具有明显的抑制活性，且显著高于重组金属蛋白酶抑制因子3。     

基质金属蛋白酶2和9与自发性胎膜早破关系的研究

目的；探讨基质金属蛋白酶2和9在自发性胎膜早破发病机制中的作用。方法：选择确诊为胎膜早破的病例39例，同期正常妊娠50倒，择期剖宫产50例。采用免疫组织化学方法检测基质金属蛋白酶2及基质全属蛋白酶9的表达情况。结果：基质金属蛋白酶2在胎膜早破产妇胎膜中的表达明显高于正常妊娠组和剖宫产组（均P＜0．01）；基质金属蛋白酶9在择期剖宫产产妇的胎膜中未见表达，而在胎膜早破组则高表达，明显高于正常产妇（P〈0．01）。结论：基质金属蛋白酶2和9在自发性胎膜早破组的高表达导致胎膜组织细胞间基质的降解，胎膜细胞间的连接强度减弱，最终发生胎膜破裂。     

内皮素受体拮抗剂对博莱霉素所致肺纤维化大鼠基质金属蛋白酶表达的影响

目的 探讨内皮素受体拮抗剂BQ-123对肺纤维化大鼠基质金属蛋白酶-1表达的影响.方法 实验分为模型组、治疗组及对照组三组.模型组用博莱霉素5 mg/kg气管内注射复制大鼠肺纤维化模型,治疗组予以内皮素受体拮抗剂BQ-123 50 μg/kg每周2次腹腔注射,对照组以等量生理盐水替代.造模后第28天处死大鼠,用半定量逆转录聚分酶链反应(RT-PCR)测定基质金属蛋白酶-1 mRNA的表达,酶联免疫吸附(ELISA)法测定基质金属蛋白酶-1蛋白的表达.结果 模型组基质金属蛋白酶-1 mRNA表达显著低于对照组(P＜0.01),治疗组较之模型组明显增加(P＜0.01).ELISA检测提示模型组基质金属蛋白酶-1蛋白含量低于对照组(P＜0.05),治疗组蛋白含量较之模型组明显增加(P＜0.01).结论 肺纤维化大鼠基质金属蛋白酶-1水平降低,应用内皮素受体拮抗剂治疗可提高基质金属蛋白酶-1的表达.     

基质金属蛋白酶-7与喉鳞癌浸润转移及预后评估的相关性

背景:基质金属蛋白酶-7在肿瘤浸润转移中具有重要作用,并与多种肿瘤的预后有关.目的:通过检测喉鳞癌组织中基质金属蛋白酶-7的表达,探讨其在喉癌浸润转移中的作用及其与预后的关系.设计:以细胞为研究对象的开放性实验研究.单位:两所大学医院的耳鼻咽喉科和一所市级医院的耳鼻咽喉科.材料:实验于2002-04/2003-01在哈尔滨医科大学附属第二医院中心实验室完成,材料为喉鳞癌和癌旁非癌组织,基质金属蛋白酶-7多克隆抗体及免疫组化试剂盒.方法:采用免疫组化方法检测70例喉鳞癌和癌旁非癌组织蜡块标本中基质金属蛋白酶-7蛋白的表达,运用反转录-聚合酶链反应和Western-blot技术检测35例喉鳞癌和癌旁非癌组织冻存标本中基质金属蛋白酶-7的表达.主要结局观察:观察基质金属蛋白酶-7的mRNA和蛋白表达结果与喉鳞癌浸润、转移及预后的关系.结果:70例喉鳞癌组织中基质金属蛋白酶-7蛋白表达阳性率为77.1%(54/70),癌旁非癌组织为5.7%(4/70)(P＜0.01).35例冻存癌组织中基质金属蛋白酶-7 mRNA的表达阳性率为74.3%(24/35),癌旁非癌组织为5.7%(2/35)(P＜0.01).基质金属蛋白酶-7蛋白和mRNA水平的表达在浸润深度为T3～T4组明显高于T1～T2组,并且与颈淋巴结转移呈明显的正相关(P＜0.01).Western-blot显示28 ku(基质金属蛋白酶-7酶原)和19 ku(活化型MMP-7)条带吸光度值与浸润深度和淋巴结转移密切相关.Kaplan-Meier生存曲线显示基质金属蛋白酶-7蛋白表达强阳性组预后较弱阳性组及阴性组恶劣(Log-rank=4.755 9,8.951 3;P=0.029 2,0.002 8).结论:基质金属蛋白酶-7与喉鳞癌的浸润、转移及预后密切相关,可作为判断喉鳞癌浸润转移潜能及预后的生物学指标.     

人胎盘天然金属蛋白酶抑制因子3的分离纯化

背景:基质金属蛋白酶是一类可促进肿瘤生长和转移的蛋白分解酶家族,其活性可被组织金属蛋白酶抑制因子所抑制。其中组织金属蛋白酶抑制因子3的抑制作用更为重要。目的:旨在从人胎盘中完全分离纯化天然组织金属蛋白酶抑制因子3,并建立组织金属蛋白酶抑制因子3酶联免疫测定方法。设计:单一样本观察。单位:沈阳医学院中心实验室。材料:人胎盘来自沈阳医学院附属奉天医院妇产科(家属知情同意);基质金属蛋白酶1来自富士药品研究所。方法:实验于2001-03/2002-05在沈阳医学院中心实验室完成。①利用4mol/L尿素Tris缓冲液(pH8.0),制备胎盘匀浆液。②匀浆液经CM52阳离子交换树脂层析和SephacrylS-200凝胶过滤二步柱层析。③SDS-聚丙烯酰胺凝胶电泳检测相对分子量及纯度。④Westernblotting鉴定纯化蛋白的性质。⑤免疫荧光法测定组织金属蛋白酶抑制因子3对基质金属蛋白酶1的抑制率。主要观察指标:①聚丙烯酰胺电泳法所示蛋白带相对分子质量。②Westernblot的显色结果。③组织金属蛋白酶抑制因子3对基质金属蛋白酶1的抑制率。④纯化后组织金属蛋白酶抑制因子3的回收率。结果:①人胎盘分离纯化的组织金属蛋白酶抑制因子3分为非糖化和糖化两种,相对分子质量分别为24000和27000两种。②非糖化和糖化的组织金属蛋白酶抑制因子3对基质金属蛋白酶1的抑制活性分别为1.1×1010mol/L和1.2×1010mol/L。胎盘来源的组织金属蛋白酶抑制因子3对基质金属蛋白酶1的抑制活性明显高于重组的组织金属蛋白酶抑制因子3。③二步层析后组织金属蛋白酶抑制因子3的回收率为23.4%。结论:人胎盘胞外基质来源的组织金属蛋白酶抑制因子3是由非糖基化蛋白和糖基化蛋白组成;两种纯化的组织金属蛋白酶抑制因子3对基质金属蛋白酶1具有明显的抑制活性,且显著高于重组金属蛋白酶抑制因子3。     

急性心肌梗死患者血清基质金属蛋白酶水平临床初步观察

目的:观察急性心肌梗死患者血清基质金属蛋白酶-2、9的水平变化,评价其临床意义。方法:入选73例急性心肌梗死患者和81例正常对照者,以双抗体夹心酶联免疫法测定该人群血清基质金属蛋白酶-2、9水平。结果:急性心肌梗死组血清基质金属蛋白酶-2、9水平明显高于对照组(P<0.01)。结论:血清基质金属蛋白酶-2、9在急性心肌梗死患者中明显升高,提示可作为急性心肌梗死的一个预测信号。     

重组组织型纤溶酶原激活物对脑缺血再灌注损伤大鼠基质金属蛋白酶9表达的影响

目的：探讨大鼠局灶性脑缺血中应用重组组织型纤溶酶原激活物溶栓引起再灌注损伤及出血性转化过程中基质金属蛋白酶9的表达。方法：2004-01／06在烟台大学药理学实验室将Wistar雄性大鼠24只随机分成两组。溶栓组12只：制作大鼠自体血栓性大脑中动脉缺血模型，2h后静脉注入重组组织型纤溶酶原激活物(10mg／kg)；线栓法缺血再灌注组12只：线栓法制作模型，在2h后抽出栓线，然后注入生理盐水。分别用免疫组织化学方法分析两组缺血后24h基质金属蛋白酶9的表达。结果：23只大鼠进入结果分析。缺血后24h两组均有基质金属蛋白酶9的表达，但是溶栓组基质金属蛋白酶9表达(45．52&;#177;4．99)明显高于线栓法缺血再灌注组(81．32&;#177;9．01)。结论：重组组织型纤溶酶原激活物溶栓导致再灌注损伤中基质金属蛋白酶9表达明显上调，其机制有待进一步研究。     

Sodium Hypochlorite and Chlorhexidine Downregulate MMP Expression on Radicular Dentin

ObjectiveMatrix metalloproteinases (MMPs) are present in radicular dentin and can convert structural matrix proteins into signaling molecules; thus, these enzymes play an essential role in dentin biomineralization and tissue regeneration therapies. Their expression on radicular dentin may be affected by the irrigation solutions used during root canal treatments. This study aimed to evaluate the effects of the most common irrigants on radicular dentin MMP expression.Materials and MethodsThe experimental solutions were distilled water (control), 5% sodium hypochlorite (NaOCl), 18% ethylenediaminetetraacetic acid (EDTA), and 2% chlorhexidine (CHX). Samples were prepared from extracted human teeth. For zymography analysis, root sections were powderized, and dentin proteins were extracted to observe gelatinolytic activity. Root dentin slices were treated with the experimental solutions for immunohistochemical analysis using anti-MMP-2 and anti-MMP-9 antibodies. ANOVA and the Tukey test were performed.ResultsZymograms revealed the presence of MMP-2, MMP-8, and MMP-20 in the control group and the EDTA-treated group. Immunohistochemistry confirmed the presence of MMP-2 and MMP-9 mainly associated with the dentinal tubule lumens and occasionally with intertubular dentin. NaOCl- and CHX-treated groups showed lower expression of MMPs than the control group. Immuno­staining for both proteinases in the EDTA-treated group showed higher expression compared to the other experimental groups.ConclusionOur results showed that most common irrigants affect MMP expression on radicular dentin. Treatment with NaOCl and chlorhexidine resulted in lower expression of MMPs, while EDTA increased their expression in root canal dentin.     

基质金属蛋白酶在冠状动脉内膜增厚中的作用研究

目的：通过检测特发性扩张性心肌病（DCM）冠状动脉的内膜增厚程度、基质金属蛋白酶（matrix metalloproteinases,MMPs）的表达,研究MMPs与冠状动脉内膜增厚的关系。方法：解剖20例病理诊断为DCM的心脏移植术受体心脏的冠状动脉,测量冠脉中层和内膜层的面积,用Westernblot检测冠状动脉壁的中层和内膜层组织中MMP1、2、3、9、13和14的蛋白表达水平。结果：DCM的冠脉均存在不同程度的内膜层增厚,增厚的内膜为细胞纤维性。内膜与中层面积比平均为0．83±0．33。冠脉的内膜与中层面积比和MMP3蛋白（r=-0．62,P〈0．005）及MMP-9蛋白（r=-0．47,P〈0．05）的表达呈负相关;MMP-1、2、13和14蛋白表达和年龄与冠脉内膜增厚无显著相关。结论：MMP-3和MMP9的表达降低促进DCM冠状动脉内膜增厚。     

A correlation between knee cartilage degradation observed by arthroscopy and synovial proteinases activities

OBJECTIVE: A novel study has been carried out to characterize the amount and activity levels of metalloproteinases (i.e., MMP-1, MMP-2, MMP-3, MMP-8, MMP-9 and MMP-13) and of their inhibitors (i.e., TIMP-1 and TIMP-2) in synovial fluid from patients (n = 56) with different degrees of either chondral lesions or knee arthritis identified and classified by arthroscopy. DESIGN AND METHODS: Zymographies, Western blotting and ELISA tests have been used to correlate the disease stage, as determined by arthroscopy, and both the amount and the activation state of different MMPs and of their inhibitors. RESULTS: Analysis of data obtained demonstrates that the degree of cartilage degradation, as seen by arthroscopy, is strictly related to the activity of some synovial MMPs, in particular MMP-2 and MMP-13 and on reduced inhibitory effect of MMP-2 by TIMP-2; in addition, a serine protease weighing about 125 kDa appears only in patients with severe cartilage degradation, i.e., with knee arthritis. CONCLUSIONS: On the whole, this is the first study in which an analysis of synovial MMPs/other proteinases activity and TIMPs has been strictly related to arthroscopy results in patients with different degrees of osteoarthritis. Results indicate that an imbalance between specific MMP activities and the amount of TIMPs and of its inhibitory efficiency is crucial for the disease evolution and it is related to the disease stage.     

Zymographic analysis of latent and activated forms of matrix metalloproteinase-2 and -9 in synovial fluid: correlation to polymorphonuclear leukocyte infiltration and in response to infection

BACKGROUND: Matrix metalloproteinase-2 and-9 (MMP-2, MMP-9), and gelatinase A and B participate in the degradation of the extracellular matrix proteins in a variety of inflammatory connective tissue diseases including arthritis. METHODS: Synovial fluid was collected by aseptic aspiration from patients with rheumatoid arthritis (RA), osteoarthritis (OA), gout, infected joint, septic arthritis, and systemic lupus erythematosus (SLE). Synovial fluid was subjected to cell count with polymorphonuclear leukocyte (PMN) differential, Gram staining and culture as necessary. MMP-2 and -9 were characterized by substrate gel electrophoresis (gelatin zymography) to resolve latent and activated 'partially proteolyzed' forms. RESULTS: Gelatin zymography revealed that MMP-9 (92, 130, 225 kDa) in synovial fluid was associated with extent of white blood cell infiltration specifically PMNs. In contrast, fibroblast MMP-2 (72 kDa) was present in all synovial fluids irrespective of PMN count. No MMP-9 was detected in the osteoarthritic specimen with low PMN count. Higher PMN count was associated with the presence of activated MMPs, especially in specimens that were confirmed culture positive. Activated synovial fluid MMPs persisted despite resolution of infection. DISCUSSION: Latent and activated MMP-2 and MMP-9 in synovial fluids fluctuate in proportion to PMN infiltration and specifically in response to infection. The presence of activated MMPs post-therapy would suggest that use of specific MMP inhibitors be indicated to eliminate activated MMPs that apparently persist post-infection.     

类风湿关节炎和系统性红斑狼疮患者血清基质金属蛋白酶2、9检测的意义

目的探讨基质金属蛋白酶（MMPs）在类风湿关节炎（RA）和系统性红斑狼疮（SLE）中的重要作用。方法采用酶联免疫吸附试验和酶谱分析了48例RA和27例SLE患者及186例健康对照者血清中MMP-2和MMP-9的浓度和活性。结果酶谱分析结果显示RA和SLE患者血清MMP-2和MMP-9的活性显著高于对照组（P〈0.01）。ELISA检测结果也表明RA、SLE组的MMP-2和MMP-9浓度明显高于对照组（P〈0.05）。结论MMP-2和MMP-9在RA和SLE患者血清中的水平及活性明显升高,表明MMPs在这些自身免疫疾病起一定的作用,可作为临床辅助诊断指标。     

免疫组化、明胶酶谱、Western Blot检测涎腺肿瘤中基质金属蛋白酶MMP-2、MMP-9表达的比较与评价

目的评价免疫组化、明胶酶谱、Western blot检测涎腺良恶性肿瘤中基质金属蛋白酶MMP-2、MMP-9表达的优点与局限性。方法分别运用免疫组化、明胶酶谱、Western blot对34例涎腺良恶性肿瘤进行MMP-2、MMP-9定位、半定量、定量检测和活性酶含量的分析,比较各方法检测结果的差异。结果免疫组化方法能定位、半定量检测出基质金属蛋白酶在良恶性肿瘤间的差异;Western blot能定量说明基质金属蛋白酶在良恶性肿瘤间的差异;明胶酶谱法能检测出MMP-2、MMP-9酶原和活性酶在良恶性肿瘤间的差异。结论免疫组化、Western blot、明胶酶谱三种方法结合,既发挥免疫组化细胞定位的优势,又克服了免疫组化法非精确定量的弱点,并打破其不能辨别酶原与活性酶的局限性,更加客观准确反映各型肿瘤组织中MMP-2、MMP-9的实际表达。     

不同牙尖斜度带桩嵌体修复下后牙短冠的有限元应力分析

背景：目前临床着重于研究带桩嵌体的材料和桩长度,而对其面形态的研究较少。目的：采用三维有限元方法,分析不同牙尖斜度的带桩嵌体对下颌第一磨牙残冠修复牙本质应力大小和分布的影响,探讨带桩嵌体修复下颌第一磨牙短冠的面形态设计。方法：采用CT扫描,Mimics软件及Unigraphics NX6.0建立右下颌第一磨牙带桩嵌体的三维有限元模型,包括带桩嵌体,牙冠,牙根,牙周膜,牙槽骨。在不同模型的咬合接触区,施加240N的加载力值,分析不同牙尖斜度的带桩嵌体对牙残冠修复牙本质的最大主应力,Von-mises应力峰值和分布情况。结果与结论：随牙尖斜度的增加,牙本质的各项应力峰值和应力分布范围逐渐增大。说明不同牙尖斜度的带桩嵌体对后牙残冠修复牙本质应力值和分布有较大影响。     

Thrombin suppresses matrix metalloproteinase 2 activity and increases tissue inhibitor of metalloproteinase 1 synthesis in cultured human peritoneal mesothelial cells.

OBJECTIVE: Recently, high levels of intraperitoneally generated thrombin were found in the effluent of patients treated with continuous ambulatory peritoneal dialysis (CAPD). The aim of the present study was to investigate in human peritoneal mesothelial cells (HMCs) the effect of thrombin on the activity and synthesis of matrix metalloproteinases (MMPs), which regulate the degradation of basement membrane collagen. METHODS: Cultured HMCs were isolated from omental tissue and used at confluence for the experiments. Conditioned media were obtained by incubating cells with serum-free M199 containing the relevant doses of thrombin. Activity of MMP-2 and MMP-9 were determined by an activity assay system. The antigen levels of MMPs and of the specific tissue inhibitor of metalloproteinases 1 (TIMP-1) were measured by ELISA. Northern blot analysis was applied to analyze mRNA expression of MMP-2 and TIMP-1. RESULTS: Incubation of HMCs with increasing doses of thrombin resulted in a concentration- and time-dependent suppression of MMP-2 activity. No changes in MMP-9 activity were seen. After a 48-hour stimulation period with thrombin (5 U/mL), MMP-2 activity decreased to 53% of that seen in control conditions. Antigen measurements revealed that this decrease was paralleled by a slight reduction in MMP-2 levels, which became significant at a thrombin dose of 5 U/mL [50.65 +/- 7.5 ng/10(5) cells (48 hours, 5 U/mL) vs 64.6 +/- 10.1 ng/10(5) cells (control)]. Under the same conditions, TIMP-1 levels were considerably increased [3.9 +/- 0.46 microg/10(5) cells (48 hours, 5 U/mL) vs 1.2 +/- 0.14 microg/10(5) cells (control)]. Hirudin (10 U/mL) completely inhibited the thrombin-induced effects on MMP-2 and TIMP-1 synthesis. These results were also reflected by Northern blot hybridization, where a slight decrease in MMP-2 and an increase in TIMP-1 mRNA expression were observed in response to thrombin. CONCLUSIONS: Our results suggest that high thrombin levels suppress MMP-2 activity through decreased MMP-2 and increased TIMP-1 synthesis. Thus, thrombin may promote the accumulation of basement membrane collagen. In addition to fibrin formation, this mechanism may represent a further contribution by thrombin to peritoneal thickening during CAPD.     

基质金属蛋白酶-8(MMP-8)在人牙本质龋中的表达

目的观察基质金属蛋白酶-8(MMP-8在牙本质龋损中的表达,探讨MMP-8与龋病发展的关系,希望能为龋病的预防和治疗开辟新的思路。方法标本选自因龋未经治疗的第三磨牙,按临床及X线诊断分为牙本质浅龋、牙本质深龋各10颗,无龋坏第三磨牙10颗为对照组。采用免疫组织化学方法观察MMP-8在不同牙本质龋损中表达。结果正常组MMP-8在成牙本质细胞层略有着色;牙本质浅龋组成牙本质细胞增生活跃,前期牙本质增厚,染色阳性,牙髓细胞染色加深;牙本质深龋组成牙本质细胞呈阳性表达,牙本质基质中呈散在条索性表达,牙髓组织中成纤维细胞、血管内皮细胞强阳性表达,在修复性牙本质中MMP-8表达强阳性。结论 MMP-8参与龋病的进展过程。     

Increased plasma concentration of matrix metalloproteinase-7 in patients with coronary artery disease

BACKGROUND: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers. METHODS: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method. RESULTS: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively with the number of natural killer cells in patients with stable and unstable CAD. CONCLUSION: Plasma concentrations of MMPs and TIMPs may be markers of CAD but appear to be differentially regulated.