二乙基亚硝胺诱导大鼠肝细胞癌过程中明胶酶的动态变化

目的观察肝癌形成过程中明胶酶表达(蛋白及mRNA水平)的动态变化,探索明胶酶在肝癌生长浸润中的作用。方法应用免疫组化法、明胶酶谱法和RT-PCR法对大鼠肝癌形成过程中各期明胶酶表达情况进行观察,并与正常对照组进行比较分析。结果正常肝组织及肝硬化组织内明胶酶有表达,肝癌形成后主要在癌细胞内表达;明胶酶原在正常肝组织中有低表达,诱癌过程中呈持续增高趋势;明胶酶-2 mRNA与其酶蛋白表达趋向一致。结论在肝癌形成过程中明胶酶转录和翻译水平均呈持续增高趋势。     

二乙基亚硝胺诱发大鼠肝癌的病理形态学研究

使用DEN诱发大鼠肝癌,整个诱癌过程分为非特异性药物反应、非癌性增生性改变和肝癌发生3个阶段。非癌性增生性改变表现为由各种异常肝细胞组成的增生结节和小胆管腺瘤样增生,从实验过程和形态学看,增生性改变与癌肿发生具有密切关系。依分化程度,肝癌的超微结构呈多样性改变。在1例胆管细胞癌中发现与APUDoma所见不能区别的致密核心颗粒,推测为1种特殊类型的胆管细胞癌。作者认为,DEN诱发的肝癌具有肝细胞和胆管细胞两种组织起源。     

二乙基亚硝胺诱发新生大鼠肝癌的实验模型

用肝化学致癌物二乙基亚硝胺（ＤＥＮ）按照Ｐｅｒａｉｎｏ诱癌模式建立ＤＥＮ大鼠肝癌模型，并对ＤＥＮ作用时间与次数加以改进，多阶段观察大鼠肝脏癌前期病变、冲瘤发生率及６种酶组织化学染色。结果表明本实验诱癌过程短，敏感性高，方法简单；碱性磷酸酶（ＡＫＰ）、琥珀酸脱氢酶（ＳＤＨ）及羧酸酯酶作为肝癌酶标记具有潜在的应用价值。提示以新生大鼠肝细胞活跃增生为基础的Ｐｅｒａｉｎｏ诱发肝癌模式，改进ＤＥＮ的处理方式     

二乙基亚硝胺诱发大鼠肝癌过程中肝脏胶原的动态观察

目的 动态观察大鼠肝脏癌变过程中胶原纤维的变化特点,为肝癌发病机制的研究提供参考。 方法 将50只雄性Wistar大鼠（体质量100～120 g）随机分为模型组和对照组,分别腹腔注射二乙基亚硝胺（DEN）50 mg/kg（加生理盐水至0.1 mL）或生理盐水（0.1 mL）,均每周2次,连续4周后改为每周1次,至14周停止。处死大鼠,取肝脏病变组织及周边正常组织,通过H-E染色、Masson染色、网状纤维染色观察其形态学改变;采用荧光定量PCR技术检测大鼠肝组织Ⅰ型及Ⅲ型胶原mRNA的动态表达;采用明胶酶谱法检测大鼠肝组织中基质金属蛋白酶（MMP）含量变化。 结果 DEN诱癌开始5周后大鼠肝组织肝硬化形成,14周后诱导出肝癌。相应地,肝组织内胶原沉积持续增加,癌灶内胶原含量则明显少于癌周组织,并呈进行性减少;MMP-2、MMP-9在癌周组织和癌组织中的变化趋势则与胶原含量变化相反。 结论 DEN诱导的大鼠肝脏癌变过程中,胶原纤维在肝组织中沉积增加,在肝癌组织中则减少,随着肝癌的进展,癌组织内胶原进一步减少,提示肝硬化组织癌变过程中胶原纤维可能被降解。     

981208冲剂抑制二乙基亚硝胺诱导的大鼠肝癌细胞增殖活性

目的：探讨中药981208冲剂对二乙基亚硝胺（DEN）诱癌过程中肝细胞增殖活性的影响。方法：建立DEN诱肝癌大鼠模型，采用免疫组化染色方法及计算机图像分析技术检测了981208冲剂对诱癌过程中肝细胞阳性表达细胞增殖核抗原（PCNA）、H－ras蛋白及诱癌后期溴化脱氧尿嘧啶（Brd-U)细胞标记指数的影响。结果：DEN诱肝癌过程中，PCNA、H-ras阳性表达呈逐渐增加趋势，两表达显正相关。981208冲剂可明显抑制诱癌过程中两蛋白的阳性表达，显降低诱癌后期Brd-U细胞标记指数。结论：中药981208冲剂可抑制大鼠肝癌形成过程中肝细胞增殖活性，从而延缓肝细胞癌变的过程。     

二乙基亚硝胺诱发大鼠肝癌癌变过程中肝细胞超微结构的变化

报道二乙基亚硝胺诱发Sprague-Dawley(SD)大鼠肝癌发生过程中肝细胞超微结构的动态改变。发现早在肉眼和光镜发现肿瘤之前,肝细胞就发生了一系列超微结构改变,且观察到卵圆细胞向高度嗜硷性肝细胞、肝细胞肝癌转化的连续变化谱。     

硒对二乙基亚硝胺诱发大鼠肝癌生长的抑制作用的观察

观察硒对二乙基亚硝胺诱发大鼠肝癌的影响。方法；在诱癌过程中，大鼠分别投予含０．２，１．０，３．０×１０＾－６硒的饲料，检测血，肝组织ＬＰＯ，ＧＳＨ－ＰＸ活性，观察诱癌率及癌结节面积。结果：补Ｓｅ后对诱癌率无显著影响，但补充３．０×１－０＾－６Ｓｅ可使癌结节面积显著减少。补Ｓｅ可显著地减轻诱癌早期血和肝组织中ＬＰＯ的形成及诱癌过程中血和肝组织中ＧＳＨ－ＰＸ活性的降低。     

二乙基亚硝胺诱发大鼠肝癌过程中超微结构的动态观察

目的 探讨肝细胞癌变过程中超微结构变化特点。方法 对二乙基亚硝胺诱癌中大鼠肝脏不同病变阶段的超微结构进行动态观察。结果 在诱癌的早、中、晚期发展过程中，损伤肝细胞的核、核仁、胞浆内糖原以及胞浆内细胞器，如线粒体、粗面内质网和滑面内质网等的变化有一定规律。结论 随诱癌时间延长，肝细胞逐渐出现变性、异型乃至癌细胞的阶段性超微结构特征。     

二乙基亚硝胺诱导大鼠肝癌模型的建立及评价

目的：探讨二乙基亚硝胺诱发大鼠肝癌模型的方法。方法：选取体重150～200 g的雄性Wistar大鼠120只,随机分为建模组和对照组。建模组实验大鼠以25 mg/kg的剂量进行二乙基亚硝胺腹腔注射,每周3次,并喂饲含30%酪蛋白和0.05%苯巴比妥钠的饲料。对照组大鼠以建模组的剂量和注射频率用生理盐水进行腹腔注射。在实验第10～18周,每隔2周对实验大鼠肝脏的肿瘤发病情况进行影像检查,将检查结果为阳性的大鼠处死做解剖分析,检查结果为阴性的大鼠继续饲养。结果：在18周时诱癌成功率为76.67%,病理学结果显示,建模组实验大鼠肝脏的病变包括了肝细胞的损伤坏死期、增生硬化期和癌变期。结论：通过长时间多次小剂量二乙基亚硝胺腹腔注射的方法,成功建立了二乙基亚硝胺的大鼠肝癌模型,此模型是研究人体肝癌成因及发展的理想可靠的活体动物模型。     

三种不同剂量二乙基亚硝胺诱癌效果比较

目的:观察不同剂量二乙基亚硝胺(DEN)诱发大鼠肝癌效果,确定合适诱癌剂量。方法:将96只100～150g Wistar SPF级雄性大鼠随机分为DEN自由饮水40ppm(A组)、64ppm(B组)、80ppm(C组)及自来水自由饮用组(D组),每组24只,普通饲料喂养,于第16周各组处死12只,取肝组织,观察肝脏形态以及成癌情况,送检病理。各组剩余12只用于观察生存期。结果:第16周诱癌各组未见1例大鼠死亡。病理学检查证实A、D组成癌率为0,B、C组诱癌率分别为83.33%、91.66%,两组成癌率比较无统计学差异;C组可见一巨块型肝癌,A组均表现为肝细胞炎症、水肿、点状坏死、结缔组织轻度增生,小灶脂肪变性。B组肝脏表面弥漫性出现局灶区域肝细胞非典型性增生,癌周结缔组织增生,未发现典型肝硬变表现,C组癌周组织肝细胞弥漫性水肿变形、点状坏死、汇管区炎细胞侵润、结缔组织增生,肝小叶结构大部分破坏。DEN诱发的肝癌为肝细胞癌。结论:以64ppm、80ppm DEN均可作诱癌剂量,64ppm诱癌在生存期方面优于80ppm,64ppm浓度诱癌是一种较理想的用于药物疗效评价的大鼠肝癌模型。     

大鼠宫颈MMP-2、MMP-8动态表达的研究

目的 通过检测大鼠宫颈基质金属蛋白2(MMP-2)、基质金属蛋白8(MMP-8)的动态表达,探讨胶原降解与宫颈成熟的关系.方法 清洁级大鼠分为未孕动情间期、妊娠10d、妊娠16d、妊娠19d和分娩后即刻组,每组各6只.宫颈称湿重.HE 常规染色显示宫颈大体结构,VG染色进行胶原纤维和肌纤维显色,免疫组织化学染色显示MMP-2、MMP-8.结果 (1)HE染色显示大鼠宫颈主要由大量纤维(胶原纤维和肌纤维)组成,分娩后即刻组宫颈间质见少量中性粒细胞.其余组未见中性粒细胞.(2)临产前宫颈湿重已有增加,至分娩后即刻增加更明显.(3)宫颈纤维组织由胶原纤维和平滑肌纤维组成,所占比例无明显差别.分娩后即刻组胶原纤维和肌纤维排列较非分娩时松散.(4)MMP-2(棕染)在所有组别间质均有表达,鳞状上皮无表达,胶原纤维、平滑肌纤维、上皮及少量血管壁呈阳性表达;妊娠19d和分娩后即刻组阳性表达的密度较其他组增强.(5)分娩后即刻组MMP-8染色见间质散在中性粒细胞棕染.其他组的组织或细胞均未见阳性表达.结论 宫颈成熟后,官颈纤维组织松散、断裂,中性粒细胞由外源性血管浸润到宫颈间质,这一变化在分娩时尤其明显;MMP-2、MMP-8这两种不同来源的基质金属蛋白酶共同降解了宫颈纤维,导致宫颈软化、扩张.

Abstract：

Objective To elucidate the relationship between collagen degradation and cervical ripening by detecting dynamic expressions of matrix metalloproteinases 2 (MMP-2) and 8 (MMP-8) in rat cervix. Method SPF rats were divided into 5 groups (n=6), namely non-pregnancy estrus interval group, gestational days 10, 16, and 19 groups, and immediately postpartum group. The wet weight of the cervix was measured and HE staining was used to display the general structure of the cervix. VG staining was applied to visualize the collagen fibers and muscular fibers. Immunohistochemistry was performed to observe the expressions of MMP-2 and MMP-8 in the cervix. Results HE staining showed that the rat uterine cervix consisted mainly of ?broblasts and ?brous connective tissues. A small quantity of neutrophils could be seen in the cervix stroma of the rats immediately after immediately parturition, but not at the other time points. The wet weight of the antepartum cervix had increased, and a more obvious increase was seen in the wet weight of the cervix immediately after parturition. The collagen fibers of the cervix consisted of collagen fibers and smooth muscle fibers, and their proportions showed no significant variation at the time points around the parturition. Immediately after parturition, the collagen fibers and muscular fibers in the cervix became loosened as compared with that before parturition. MMP-2 expression was found in the cervical stroma but not in the squamous epithelium in nonpregnancy, term pregnancy, and immediately after parturition; the smooth muscle cells, vascular wall, and stromal ?broblasts showed positive expression of MMP-2. Enhanced intensity of MMP-2 staining was seen in term pregnancy and postpartum group in comparison with that in the other groups. MMP-8 expression was observed in the cervix of rats immediately after parturition, with scattered neutrophils positive for MMP-8 spotted in the stroma of the ripened cervix. MMP-8 expression was not detected in the other groups. Conclusion Ripened cervical fibrous tissue becomes loose and broken, and cervical ripening is accompanied by infiltration of neutrophils from exogenous vessels. These changes are particularly evident after parturition. MMP-2 and MMP-8 cooperate to degrade the cervical fibers, leading to cervical softening and expansion.     

缺血再灌注大鼠脑内基质金属蛋白酶的动态变化

目的 研究局灶性脑缺血再灌注后基质金属蛋白酶(MMPs)的变化。方法 应用含明胶的定量酶谱技术,检测大鼠局灶性脑缺血再灌注7 d内MMP-2和MMP-9的表达。结果 MMP-9(92 kd)在假手术组和手术组非缺血侧没有或仅有极低量的表达,手术组缺血侧再灌注3 h后开始出现MMP-9表达,24、48 h较假手术组显著升高(P<0.05,P<0.01),并显著高于其它各组(P<0.05)。MMP-2(72 kd)在各组缺血侧与非缺血侧均有表达,48 h缺血侧开始较假手术组升高(P<0.05),7 d到达高峰;3 h和24 h与7 d相比,有显著性差别(均P<0.01)。各组非缺血侧之间无显著差别(P>0.05)。结论 脑缺血再灌注后MMP-9和MMP-2的水平升高;MMP-9上调可能与缺血再灌注后的炎症损伤有关,MMP-2可能与炎症反应损伤后的修复过程相关。     

缺血再灌注大鼠脑内基质金属蛋白酶的动态变化

目的研究局灶性脑缺血再灌注后基质金属蛋白酶(MMPs)的变化.方法应用含明胶的定量酶谱技术,检测大鼠局灶性脑缺血再灌注7 d内MMP-2和MMP-9的表达.结果MMP-9(92kd)在假手术组和手术组非缺血侧没有或仅有极低量的表达,手术组缺血侧再灌注3 h后开始出现MMP-9表达,24、48 h较假手术组显著升高(P<0.05,P<0.01),并显著高于其它各组(P<0.05).MMP-2(72kd)在各组缺血侧与非缺血侧均有表达,48 h缺血侧开始较假手术组升高(P<0.05),7 d到达高峰;3 h和24 h与7 d相比,有显著性差别(均P<0.01).各组非缺血侧之间无显著差别(P>0.05).结论脑缺血再灌注后MMP-9和MMP-2的水平升高;MMP-9上调可能与缺血再灌注后的炎症损伤有关,MMP-2可能与炎症反应损伤后的修复过程相关.     

Dynamic changes of MAPK signaling during DEN-induced rat hepatocellular carcinoma occurrence and development

Objective:To investigate the expression levels of total and phosphorylation p38,JNK and ERK1/2 protein during diethylnitrosamine(DEN)-induced rat hepatocellular carcinoma occurrence and development.Methods:To induce hepatocellular carcinoma,we performed intermittently administrated DEN to rats.Using light microscopy and electron microscopy technique to discover that liver tissue morphological changes in the process.And then the expression of p38,JNK,ERK1/2 mRNA and protein was performed by RT-PCR and western blot analysis,in order to furthermore explore the association of them.Results:In rat hepatoma model development,protein of p-p38、p-ERKl/2、p-JNK and its mRNA expression were significantly increased with increasing treatment time,but,no significant changes of p38,ERK,of JNK protein and its mRNA expression.Conclusions:During DEN-induced rat hepatocellular carcinoma,p-p38 and p-ERK proteins expressed lower and p-JNK protein expressed high,and its expression was positively correlated with the development of hepatocellular carcinoma.     

基质金属蛋白酶在分娩中的表达及其意义

目的探讨基质金属蛋白酶在分娩机制中的作用.方法采用蛋白电泳法测定40例(自然分娩和剖宫产各20例)血清基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)蛋白的活性变化及表达情况.结果自然分娩组和剖宫产组MMP-9酶原形式的表达分别为14970.33±1891.20和11626.80±2161.75,MMP-9活性形式分别为35523.17±6820.10和25972.13±4615.03;MMP-2酶原形式分别为19858.40±4030.78和12542.33±1607.20,MMP-2的活性形式分别为26909.33±2976.38和15120.50±2421.03.自然分娩组和剖宫产组比较均具有显著性差异(P＜0.05).结论MMP-9和MMP-2蛋白在自然分娩中表达高于剖宫产,提示自然分娩MMP-9和MMP-2蛋白使宫颈的胶原分解,并促使宫颈成熟和扩张.     

MMP-2,MMP-9,TIMP-1和TIMP-2在肝癌中原位表达

目的 :探讨肝癌中基质金属蛋白酶MMP 2 ,MMP 9和组织金属蛋白酶抑制剂TIMP 1 ,TIMP 2的mRNA和蛋白质表达与临床病理特征和预后的关系。方法 :在 5 6例有完整随访资料的原发性肝癌标本中原位杂交检测MMP 2mRNA ,TIMP 2mRNA ;免疫组化检测MMP 2 ,MMP 9,TIMP 1 ,TIMP 2蛋白质的表达。结果 :MMP 2mRNA ,TIMP 2mRNA ,MMP 2 ,MMP 9,TIMP 1和TIMP 2蛋白质在肝癌中的阳性表达分别为 4 8(85 .7% )例 ,35 (6 2 .5 % )例 ,4 4 (78.6 % )例 ,4 1 (73.2 % )例 ,30 (5 3.6 % )例 ,38(6 8% )例。MMP 2mRNA ,MMP 2 ,MMP 9在肝癌中呈高表达 ,而TIMP 1蛋白呈低表达 (P <0 .0 1 ,P <0 .0 5 )。TIMP 2mRNA与TIMP 2蛋白 ;MMP 2mRNA与MMP 2蛋白在肝癌中的表达呈正相关 (分别为r=0 .31 6 ,P <0 .0 5 ;r=0 .35 6 ,P <0 .0 5 )。MMP 2mRNA的表达与肝癌肿瘤大小和临床分期呈正相关 (分别为r =0 .4 4 1 ,P <0 .0 1 ;r=0 .340 ,P <0 .0 5 ) ;MMP 9蛋白表达阳性的肝癌患者术后生存时间缩短 (P <0 .0 5 )。Kaplan Meier单因素分析发现MMP 2 ,MMP 9表达阳性患者的预后差 (P <0 .0 1 ,P <0 .0 5 )。多因素Cox回归分析显示MMP 2 ,MMP 9的蛋白表达可作为肝癌估测预后的指标。结论 :基质金属蛋白酶MMP 2 ,MMP 9的过表达以及其与TIMP 2 ,MMP     

MMP—2，MMP—9，TIMP—1和TIMP—2在肝癌中原位表达

OBJECTIVE: To explore the expression and clinical prognostic significance of matrix metalloproteinase-2 mRNA (MMP-2 mRNA), tissue inhibitor of matrix metalloproteinase-2 mRNA (TIMP-2 mRNA), matrix metalloproteinase-2 protein (MMP-2), matrix metalloproteinase-9 protein (MMP-9), tissue inhibitor of matrix metalloproteinase-1 protein (TIMP-1), and tissue inhibitor of matrix metalloproteinase-2 protein (TIMP-2) in the hepatocellular carcinomas (HCCs). METHODS: Fifty-six specimens of HCCs from 56 patients, who were followed-up, were investigated by in situ hybridization with specific probes for MMP-2, TIMP-2, and by immunohistochemistry with anti-MMP-2, MMP-9 and anti-TIMP-1, TIMP-2 monoclonal antibody. We analyzed the data with chi-square test, spearmans correlation analysis, monovariate Kaplan-Meier plot and multivariate Cox regression analysis. RESULTS: 1. The positive expression of MMP-2mRNA, TIMP-2mRNA, MMP-2 protein, MMP-9 protein, TIMP-1 protein and TIMP-2 protein in the 56 HCCs cases were 48 (85.7%), 35 (62.5%), 44 (78.6%), 41 (73.2%), 30 (53.6%), and 38 (68%), respectively. 2. We found over-expression of MMP-2 mRNA, MMP-2 protein, and MMP-9 protein, but low expression of TIMP-1 protein in the 56 cases of HCCs (P < 0.01, P < 0.05). 3. There was a positive association between TIMP-2mRNA and TIMP-2 protein expression, and between MMP-2 mRNA and MMP-2 protein in HCCs, respectively (r = 0.316, P < 0.05; r = 0.356, P < 0.05). 4. Over-expression of MMP-2 mRNA was positively correlated to the tumor size and TNM classification (r = 0.441, P < 0.001; r = 0.340, P < 0.05), and MMP-9 protein was related to shortened survival (P < 0.05). 5. In both monovariate Kaplan-Meir plot and multivariate Cox regression analysis, the expression of MMP-2 protein and MMP-9 protein were linked to unfavorable prognosis. These results were further confirmed by multivariate analysis in which MMP-2 protein and MMP-9 protein emerged as independent prognostic factors for poor survival regardless of the age, tumor size, tumor grades, TNM classification and expression of MMP-2mRNA, TIMP-2mRNA, TIMP-1 protein and TIMP-2 protein. The hazard ratios of expression of MMP-2 protein and MMP-9 protein were 3.875 and 4.528, respectively. CONCLUSION: The over-expression of MMP-2mRNA, MMP-2 protein and MMP-9 protein and the imbalance between MMP-2 and TIMP-2 play pivotal roles in the degradation of excellular matrix of HCCs. MMP-2 and MMP-9 immunoreactive protein have been closely related to a shortened survival independent of major prognostic indicators in the primary HCC and increase the risk of the patients after the operation.     

大鼠急性心肌梗死后心室重构进展中基质金属蛋白酶活性的变化

目的　探讨大鼠急性心肌梗死 (AMI)后心室重构进展中基质金属蛋白酶 (MMPs)活性的变化与心功能的关系。方法　雄性SD大鼠随机分为假手术组和手术组 (结扎大鼠冠状动脉前降支制作AMI模型 ) ,再进一步分为 1、7、14、2 8、4 2d亚组。应用心脏超声和血流动力学测定心功能和心室重构 ;采用明胶酶法测定左室心肌MMPs活性。结果　手术组大鼠术后 14d起左室舒张末期直径 (LVEDD)逐渐增加 ,左室射血分数(LVEF)及左室短轴缩短率 (FS)逐渐降低 ,至 4 2d最明显 ;术后 1d起左室舒张末压 (LVEDP)逐渐升高 ,左室压力上升最大速率 (dp/dtmax)及压力下降最大速率 (dp/dtmin)逐渐下降 ,以术后 4 2d最明显 ;术后 1dMMP2 和MMP9活性即升高 ,至 7d时活性最高 ,此后逐渐下降 ,与相应时段假手术组比较 ,差异均有显著性 (P值均 <0 .0 1)。MMP2 活性与LVEDD成正相关 (r =0 .92 ,P <0 .0 1) ;与FS、LVEF、dp/dtmax成负相关 (r =- 0 .91、- 0 .88、- 0 .87,P <0 .0 5～ 0 .0 1)。MMP9活性与LVEDD成正相关 (r =0 .92 ,P <0 .0 1) ;与FS、LVEF、dp/dtmax成负相关 (r =- 0 .95、- 0 .96、- 0 .94 ,P值均 <0 .0 1)。结论　大鼠AMI后MMP2 、MMP9活性增加呈动态变化 ,并与心功能、心室重构相关 ,提示它们在促进AMI后心室重构、心功能异常     

基质金属蛋白酶9与血浆脑钠素在大鼠急性心肌梗死后的表达

目的:研究急性心肌梗死(AMI)后血浆脑钠素(BNP)与基质金属蛋白酶9(MMP-9)的表达变化及相关关系,探讨血浆BNP浓度与AMI后左室重构的关系.方法:SD大鼠随机分为对照组、心肌梗死后1 d组、心肌梗死后1 w组、心肌梗死后2 w组、心肌梗死后4 w组.结扎大鼠冠状动脉前降支制作AMI模型.行血流动力学检测后,测定各组大鼠血浆BNP浓度及MMP-9,后处死大鼠,取心肌标本测定梗塞面积及心肌胶原含量.结果:心肌梗死各组较对照组左心室舒张末压均显著增加(P＜0.05),平均动脉压、左心室内压最大上升和下降速率则显著降低(P＜0.01);第4周组左心室湿重较其余各组明显增加(P＜0.01).心肌梗死各组BNP、MMP-9表达较同期对照组显著增加(P＜0.01),MMP-9与BNP呈正相关(r=0.81,P＜0.01);心肌胶原含量增加,与左心室内压最大上升和下降速率呈负相关.结论:心梗后BNP与MMP-9明显升高呈动态改变,并且与心室重构及心功能密切相关,心梗后BNP的迅速分泌可能是促进MMP-9表达的原因之一;心梗后同时测定BNP与MMP-9浓度对于判断心功能及心室重构从而间接判断预后有重要意义.