替米沙坦上调3T3-L1脂肪细胞脂联素表达的机制

目的探讨过氧化物酶体增殖物活化受体γ(PPARγ)在替米沙坦调节脂肪细胞脂联素表达中的作用。方法体外培养3T3-L1脂肪细胞,采用替米沙坦(10μmol/L)和/或PPARγ阻断剂GW9662(30μmol/L)干预3T3-L1脂肪细胞,采用实时定量RT-PCR和Westernblot方法检测3T3-L1脂肪细胞的脂联素表达水平。结果与空白对照组相比,经GW9662干预后3T3-L1脂肪细胞脂联素mRNA表达水平明显降低(P<0.05);替米沙坦组脂联素mRNA和蛋白表达水平明显增加(P<0.05);替米沙坦+GW9662组(替米沙坦+GW组)脂联素mRNA和蛋白表达水平有增高趋势,但与空白组相比无统计学差异(P>0.05)。结论 PPARγ活性在替米沙坦上调3T3-L1脂肪细胞脂联素表达过程中可能起着一定程度的作用。     

RNA干扰PPAR-α基因表达对HepG2细胞部分脂代谢信号及炎症因子IL-6的影响

目的研究RNA干扰抑制PPAR-α基因表达对Hep G2部分脂代谢信号及炎症因子IL-6影响。方法在脂质体lipofectamineTM2000介导下将PPAR-αsi RNA瞬时转入人肝细胞癌Hep G2细胞,用RT-PCR方法检测转染效率及转染后LPL m RNA、IL-6m RNA、CPT-1 m RNA的表达变化。结果成功转染PPAR-αsi RNA后,与空白对照组比,转染试剂组Hep G2细胞LPL m RNA表达增高（0.002605±0.000213 vs 0.003920±0.000324,P〈0.05）、CPT-1m RNA表达稍降低（2.25831±0.06151 vs 2.06625±0.05091）,差异无统计学意义,IL-6m RNA表达显著增高（0.01604±0.00118 vs 0.02458±0.001718,P〈0.01）。结论在人肝细胞癌Hep G2细胞中抑制PPAR-α基因表达可促进LPL m RNA、IL-6 m RNA表达,促进脂蛋白酯酶合成而诱发炎症,但对线粒体氧化途径的关键酶CPT-1表达无明显影响。     

柚皮苷及柚皮素对高脂模型大鼠单核细胞过氧化物酶体增殖物激活受体-δ水平的影响

目的：探讨黄酮类化合物柚皮苷及柚皮素对高脂模型大鼠单核细胞过氧化物酶体增殖物激活受体-δ（peroxisome proliferator-activated receptors δ,PPAR-δ）水平的影响。方法：实验动物分为普通饲料组,高脂饲料对照组,柚皮苷和柚皮素高剂量及低剂量组。除普通饲料组外,其余各组通过高脂乳剂灌胃,建立高脂模型。然后再分别给予0.5%的羧甲基纤维素（CMC）或不同剂量的柚皮素或柚皮苷灌胃8周。实验结束后应用RT-PCR法检测外周血单核细胞PPAR-δ的表达,测定血中甘油三脂、总胆固醇、高密度脂蛋白、低密度脂蛋白及极低密度脂蛋白的水平。结果：与高脂饲料对照组相比,高剂量柚皮苷和柚皮素组血中甘油三脂、总胆固醇、低密度脂蛋白及极低密度脂蛋白的水平降低,差异有统计学意义（均P〈0.05）;高密度脂蛋白水平明显升高（P〈0.05）;高剂量柚皮素及柚皮苷组外周血单核细胞PPAR-δ mRNA的表达高于高脂饲料对照组,差异有统计学意义（均P〈0.05）;相关性分析结果表明PPAR-δ与甘油三脂（r=0.158, P〈0.05）、总胆固醇水平（r=0.147, P〈0.05）呈正相关。结论：高剂量的柚皮苷与柚皮素可降低血脂水平,上调PPAR-δ的表达。     

替米沙坦苯那普利治疗轻中度高血压疗效比较

替米沙坦是国产血管紧张素Ⅱ(AT-Ⅱ)受体拮抗剂类的口服抗高血压药物,它在减少血管紧张素转换酶抑制剂最常见的干咳副作用的同时,阻断肾素-血管紧张素-醛固酮系统更完全.本文通过替米沙坦和苯那普利的对照研究,来评价替米沙坦的抗高血压的疗效.     

替米沙坦对慢性心力衰竭患者神经内分泌激素的影响

目的 探讨替米沙坦对慢性心力衰竭患者神经内分泌激素的影响.方法 将96例慢性心力衰竭患者(心功能Ⅱ～Ⅳ级)随机分为两组,分别接受替米沙坦、贝那普利治疗.放射免疫法测定治疗前、治疗3个月后血浆去甲肾上腺素、肾素、血管紧张素Ⅱ、醛固酮及内皮素水平的变化.结果 替米沙坦、贝那普利治疗后血浆去甲肾上腺素、内皮素水平均有明显下降(P＜0.01);贝那普利组血浆肾素、血管紧张素Ⅱ、醛固酮水平无显著变化(P＞0.0 5);替米沙坦组血浆肾素、血管紧张素Ⅱ水平有显著下降(P＜0.01),但醛固酮水平无明显变化(P＞0.0 5).结论 替米沙坦对慢性心力衰竭患者神经内分泌激素只有部分改善作用.     

替米沙坦对高血压并不稳定型心绞痛患者血清脂联素、超敏C反应蛋白及肿瘤坏死因子表达的影响

目的探讨替米沙坦对高血压并不稳定型心绞痛患者血清脂联素（APN）、超敏C反应蛋白（hs—CRP）、肿瘤坏死因子（TNF—α）表达的影响。方法将100例高血压并不稳定型心绞痛患者按数字表法随机分为替米沙坦组（50例）和氯沙坦组（50例）,分别予以口服替米沙坦和氯沙坦治疗,均治疗8周。观察两组血压控制情况、血清APN、hs—CRP和TNF-α表达及治疗后心血管事件发生情况。结果两组治疗8周后均实现血压达标。治疗开始后,替米沙坦组APN升高较氯沙坦组快（P〈0．05）,替米沙坦组hs-CRP、TNF-α水平降低亦均较氯沙坦组快（均P〈0．05）。两组均随访4个月,替米沙坦组心血管事件发生率为10．0％（5／50）,明显低于氯沙坦组的24．5％（12／49）（P〈0．05）。结论替米沙坦对高血压并不稳定型心绞痛患者APN、hs—CRP、TNF—α表达的调节作用较氯沙坦更显著,更有利于降低此类患者的短期心血管事件发生率。     

血管紧张素Ⅱ受体拮抗药的临床应用与不良反应

随着人们对肾素-血管紧张素-醛固酮系统（RAAS）认识的不断深入，血管紧张素Ⅱ受体拮抗药（ARB）已成为一类重要的高血压治疗药物，是继血管紧张素转换酶抑制剂（ACEI）后，又一类作用于肾素-血管紧张素系统（RAS）的新型降压药，具有高效、长效、安全、可口服、耐受性好等特点。ARB属非肽类化合物，目前经美国食品与药品管理局（H）A）批准应用于临床的ARB有氯沙坦、缬沙坦、伊贝沙坦、替米沙坦、坎地沙坦、     

奥美沙坦酯对自发性高血压大鼠心室重构的影响

目的研究奥美沙坦酯对自发性高血压大鼠(SHR)心室重构及过氧化物酶体增殖物激活受体α(PPARα)、过氧化物酶体增殖物激活受体γ(PPARγ)表达的影响。方法将36只雄性SHR随机分为模型组与实验组,各18只;同时选择18只相应周龄的Wistar Kyoto(WKY)大鼠作为对照组。实验组大鼠灌胃给予奥美沙坦酯10 mg·kg^-1·d^-1,对照组与模型组均灌胃给予等量生理盐水,每天1次,均连续灌胃4周。用心脏彩色多普勒超声仪检测舒张末期室间隔厚度(IVSd)、收缩末期室间隔厚度(IVSs)、左心室舒张末期后壁厚度(LVPWd)、左心室收缩末期后壁厚度(LVPWs)与心率(HR);用苏木精-伊红(HE)染色观察大鼠心肌组织病理学变化;用放射免疫法测定血浆内皮素(ET)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)与肾素活性(PRA)含量;用蛋白质印迹(Wb)法检测心肌组织PPARα和PPARγ蛋白表达。结果对照组、模型组与实验组大鼠IVSd分别为(1.18±0.07),(3.14±0.25)和(2.21±0.19)mm;IVSs分别为(2.06±0.19),(4.19±0.36)和(3.13±0.27)mm;LVPWd分别为(1.38±0.16),(3.07±0.23)和(2.41±0.20)mm;LVPWs分别为(2.14±0.26),(4.12±0.35)和(2.98±0.31)mm;HR分别为(216.42±24.83),(425.11±46.02)和(234.69±26.15)次/分。与对照组比较,模型组大鼠IVSd、IVSs、LVPWd、LVPWs与HR及血浆ET、AngⅡ、ALD、PRA含量均显著升高,且实验组均显著低于模型组;而模型组心肌组织PPARα、PPARγ蛋白相对表达量均显著低于对照组,实验组均显著高于模型组(均P<0.05)。结论奥美沙坦酯可有效改善SHR心脏结构,同时可通过上调心肌组织PPARα和PPARγ蛋白表达,抑制心室重构,改善心脏功能。     

替米沙坦对5/6肾切除肾衰竭大鼠的肾脏保护作用及其机制研究

目的 探讨血管紧张素AT1受体拮抗剂替米沙坦对5/6肾切除肾衰大鼠的肾脏保护作用及可能作用机制.方法 选用180 ～ 200 g雄性SD大鼠30只建立5/6肾切除肾衰模型,分为假手术组、模型组和替米沙坦组,各10只.第12周时采用断头法处死大鼠,并检测各组大鼠血清尿素氮、肌酐及24h尿蛋白水平;取残余肾组织行病理检查,判断肾小球硬化、肾小管间质损伤程度;利用反转录聚合酶链反应( RT-PCR)和Western Blot检测过氧化物酶增殖体活化受体γ(PPARγ)和神经型一氧化氮合酶(nNOS)蛋白和mRNA的表达水平.结果 3组肌酐、血清尿素氮及24 h尿蛋白情况:假手术组:(35±4)μmol/L,(6.6±1.0) mmol/L,(30 ±4) mg/d;模型组:(91±10) μmol/L,(23.0±3.4)mmol/L,(96±21) mg/d;替米沙坦组(62±10) μmol/L,( 15.3 - 1.3) mmol/L,(45±17) mg/d;与假手术组相比,模型组和替米沙坦组大鼠上述指标均明显升高(P＜0.01);但与模型组相比,替米沙坦组各指标则明显降低(P＜0.05).病理学检查示模型组大鼠肾组织有明显的肾小球硬化及肾小管间质损伤,肾小球硬化指数及肾小管间质损伤指数均较假手术组明显增高(P＜0.01);而替米沙坦组上述指标则较模型组明显降低(P＜0.05).Western Blot和RT-PCR显示模型组PPARγ、nNOS蛋白和mRNA的表达较假手术组明显下降(P＜0.05),而替米沙坦组PPARγ和nNOS的表达则较模型组明显升高(P＜0.05).结论 大鼠5/6肾切除后,给予替米沙坦可以明显减轻肾小球硬化和肾间质纤维化的程度,其作用机制可能与其上调PPARγ和nNOS基因的表达有关,且二者有明显的相关性.     

替米沙坦对急性心肌梗死患者冠状动脉介入治疗后心室重塑的影响

目的探讨替米沙坦对急性心肌梗死患者行紧急冠状动脉介入治疗（PCI）后左心室重塑的影响。方法选择行急诊PCI的急性心肌梗死患者80例,随机分为2组,40例术后当天开始服用替米沙坦为替米沙坦组（80mg,1次/d）,40例服培哚普利（4mg,1次/d）作为对照组,观察9个月,分别于治疗后第1天、第9个月比较2组心脏超声各项指标和血清内皮素-1、一氧化氮（NO）及白介素-6水平的变化。结果与对照组比较,治疗后替米沙坦组内皮素-1、白介素-6明显降低,NO水平升高,左心室收缩末容积、左心室舒张末容积显著改善,左心室射血分数（LVEF）提高,室壁瘤的发生减少（P均〈0.05）。结论替米沙坦能明显改善急诊PCI后急性心肌梗死患者左心室重塑及血管内皮功能。     

Telmisartan inhibits vascular dysfunction and inflammation via activation of peroxisome proliferator-activated receptor-γ in subtotal nephrectomized rat

Telmisartan, an angiotensin II type 1 receptor blocker, reportedly exhibits a partial peroxisome proliferator-activated receptor (PPAR)-γ agonistic action. To test whether telmisartan ameliorates vascular injury in the chronic kidney disease model rat through the PPAR-γ pathway, telmisartan (5 mg/kg per day, orally), losartan (5 mg/kg per day, orally) or telmisartan plus PPAR-γ antagonist, GW9662 (1 mg/kg/day, i.p.), was administered for 14 days to subtotal nephrectomized rats (Nx). There was no significant difference in systolic blood pressure or fasting blood glucose values among all groups. Subtotal nephrectomy significantly aggravated the levels of urinary protein excretion, blood urea nitrogen and plasma malondialdehyde concentration, which were attenuated by telmisartan or losartan treatment. Vasodilation in response to acetylcholine in the aortic ring was impaired in the Nx, and improved by treatment with telmisartan. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin and vascular cell adhesion molecule-1 were enhanced in the Nx aorta and the overexpression was suppressed by telmisartan. The increased NADPH oxidase-derived superoxide production in the aorta from the Nx rat was suppressed by telmisartan. Cotreatment with GW9662 partly blunted the normalization of vascular dysfunction and inflammation. While losartan also attenuated these vascular changes in the Nx rats, the extent of the attenuation was significantly greater in the telmisartan-treated group than in the losartan-treated group. These results suggest that, in addition to a class effect of angiotensin II type 1 receptor blockers, telmisartan exerted vasoprotective effects through its PPAR-γ agonistic property in rats with renal failure.     

Effects of telmisartan and valsartan on insulin sensitivity in obese diabetic mice

Telmisartan and valsartan have angiotensin II receptor blocking activity. Because telmisartan has also an agonistic action for peroxisome proliferators-activator receptor (PPAR)-γ, it is speculated that an effect of telmisartan on insulin sensitivity is different from that of valsartan, which lacks of PPAR-γ agonistic activity. To address the issue, effects of telmisartan and valsartan on insulin sensitivity, adipocytokines and PPAR-γ target genes were evaluated in obese diabetic mice. KK-A^y mice were treated with telmisartan (5 mg/kg) and valsartan (15 mg/kg), once daily for 3 weeks. Insulin tolerance test was performed on day14, and plasma adiponectin concentration and mRNA expression levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in adipose tissues were measured on day 21. Time-course of plasma glucose level after the injection of insulin in mice with telmisartan was not significantly different from that of animals with valsartan. In addition, PPAR-γ antagonist did not diminished the improvement of insulin sensitivity by telmisartan. Telmisartan and valsartan elevated plasma adiponectin concentration and suppressed the mRNA expressions of TNF-α and IL-6 in adipose tissues. These variables of the telmisartan- and valsartan-treated groups did not significantly differ. Influence of telmisartan on the PPAR-γ target genes (ap2 and fatty acid synthase) mRNA expressions was not detected in adipose tissues under the present condition. These data suggest that the effect of telmisartan on insulin sensitivity is similar to that of valsartan, and a role of PPAR-γ-mediated stimuli is small in the telmisartan-induced improvement of insulin sensitivity.     

Clinical Trials Reports: Ongoing and planned clinical trials of antiarrhythmic drugs:Cardiovascular & Renal

The discovery that the insulin-sensitising thiazolidinediones (TZDs), specific peroxisome proliferator-activated receptor-γ (PPARγ) agonists, have antiproliferative, anti-inflammatory and immunomodulatory effects has led to the evaluation of their potential use in the treatment of diabetic complications and inflammatory, proliferative diseases in non-insulin-resistant, euglycaemic individuals. Apart from improving insulin resistance, plasma lipids and systemic inflammatory markers, ameliorating atherosclerosis and preventing coronary artery restenosis in diabetic subjects, currently approved TZDs have been shown to improve psoriasis and ulcerative colitis in euglycaemic human subjects. These data imply that the activation of PPAR-γ may improve cardiovascular risk factors and cardiovascular outcomes in both insulin-resistant diabetic and non-diabetic individuals. Through their immunomodulatory and anti-inflammatory actions, TZDs and other PPAR-γ agonists may prove to be effective in treating diseases unrelated to insulin resistance, such as autoimmune (e.g., multiple sclerosis), atopic (e.g., asthma, atopic dermatitis) and other inflammatory diseases (e.g., psoriasis, ulcerative colitis). Newer and safer selective PPAR-γ agonists are presently under development. Furthermore, of considerable interest is the recent discovery that a unique subset of currently prescribed antihypertensive angiotensin II Type 1 receptor antagonists has selective PPAR-γ-modulating activity. These discoveries pave the way for the development of drugs for treating chronic multigenic cardiovascular and metabolic diseases, for which therapy is presently insufficient or non-existent. The potential utility of the currently available TZDs rosiglitazone and pioglitazone and PPAR-γ-modulating angiotensin II Type 1 receptor antagonists in treating cardiovascular, metabolic and inflammatory diseases in insulin resistant and euglycaemic states is of immense clinical potential and should be investigated.     

过氧化物酶体增生物激活受体γ激动剂致水肿机制及预防的研究进展

过氧化物酶体增生物激活受体γ（peroxisome proliferator-activated receptor gamma,PPAR-γ）激动剂主要包括噻唑烷二酮类（thiazolidinediones,TZDs）和非噻唑烷二酮类新型PPAR-γ激动剂。噻唑烷二酮类药物常用的有曲格列酮、吡咯列酮及罗格列酮。PPAR-γ激动剂的常见不良反应之一为水肿,并可加重或引致充血性心力衰竭。水肿发生率为3%～28.9%;PPAR-γ激动剂和其他口服降血糖药或胰岛素合用可增加水肿发生率。PPAR-γ引起水肿的机制涉及水钠潴留、血管扩张以及血管通透性增加等因素,特别是分布于远端肾小管和集合管的水、钠转运蛋白调节异常对水钠潴留的发生起重要作用。PPAR-γ激动剂引起的水肿一般较轻,停药后可消退。糖尿病合并中、重度充血性心力衰竭患者[NYHA（New York Heart Association）Ⅲ或Ⅳ级]避免用PPAR-γ激动剂,合并轻度充血性心力衰竭患者（NYHAI至Ⅱ级）应慎用,尽可能用最小剂量,必需时,剂量应逐渐增加,可联合应用利尿剂,并应严密监测患者体重和水肿的发生情况。预防治疗水肿的方法包括应用新的选择性PPAR-γ调节剂、蛋白激酶C-β或上皮细胞钠通道的特异性抑制剂及PPAR-γ拮抗剂。     

氯沙坦对原发性高血压患者血管内皮功能及炎症因子的影响

目的:探讨氯沙坦对原发性高血压患者血管内皮功能及炎症因子的影响。方法:将50例轻、中度原发性高血压患者(治疗组)给予氯沙坦50mg,qd,血压下降不理想者则增加至100mg,qd或50mg,bid,连用16周。观察治疗前、后患者血压的变化,并进行血浆内皮素1(ET-1)、一氧化氮(NO)、超敏C反应蛋白(hs-CRP)和白细胞介素6(IL-6)水平的测定。另选30例健康体检者作为对照组。结果:治疗前患者血浆NO水平较对照组明显降低,ET-1、hs-CRP和IL-6水平明显升高(P<0.01);经氯沙坦治疗16周后,治疗组收缩压和舒张压均控制正常,血浆NO水平较治疗前明显升高,ET-1、hs-CRP和IL-6水平较治疗前明显下降(P<0.01或P<0.05),但血浆NO水平仍低于对照组,ET-1、hs-CRP和IL-6水平仍高于对照组(P<0.05)。结论:氯沙坦具有良好降压效果,能明显改善原发性高血压患者内皮功能且具有抗炎作用,但无法完全逆转高血压引起的血管内皮功能改变和血浆炎症因子升高。     

Focal adhesion kinase in cancer

The metabolic syndrome (MetS) is a strong predictor of cardiovascular morbidity and mortality, as well as new Type 2 diabetes. MetS consists of visceral obesity, elevated blood pressure, impaired glucose metabolism, atherogenic dyslipidaemia (elevated triglycerides and low levels of high-density lipoprotein cholesterol), as well as other metabolic abnormalities. The underlying pathophysiology seems to be largely, but not uniquely, attributable to insulin resistance. Existing antihypertensive drugs were designed to lower blood pressure rather than to modify the metabolic abnormalities associated with hypertension. This review considers the role of renin–angiotensin system inhibition and especially the use of angiotensin receptor blockers (ARBs) in the treatment of hypertension in MetS. There are differences among ARBs. Among them is the uricosuric effect of losartan. Furthermore, telmisartan may function as a partial agonist of the peroxisome proliferator-activated receptor-γ (PPAR-γ).     

石榴花多酚对糖尿病大鼠IL-6、TXB2及PPAR-γ mRNA基因表达的影响

目的观察石榴花多酚对小剂量链脲佐菌素加高脂饲料诱导的胰岛素抵抗模型大鼠IL-6、TXB2以及心肌组织PPAR-γ mRNA基因表达的影响。方法♂SD大鼠高脂饲料喂养1mon后注射小剂量STZ,2wk后测大鼠空腹血糖,血糖值>11.1者为造模成功的大鼠,将造模成功的大鼠随机分为模型组和药物干预组,另设空白对照组,药物干预1mon,常规测定各组大鼠给药前后的空腹血糖(FPG)和给药后各组大鼠的空腹血清胰岛素水平(Fins)、IL-6、TXB2,计算胰岛素敏感性指数(ISI)、胰岛素抵抗指数(Homa-IRI),提取心肌组织总RNA,采用逆转录PCR技术扩增PPAR-γ基因片段,检测其基因表达水平。结果石榴花多酚能降低模型大鼠FPG水平和Fins、IL-6、TXB2含量,增加PPAR-γmRNA基因表达,提高ISI,降低Homa-IRI。结论石榴花多酚对大鼠IR有一定程度的改善作用,其机制可能与提高IR大鼠心肌组织PPAR-γ基因的表达有关。     

冠心病患者血清SAA、IL-6、TNF-α和hs-CRP检测及临床意义探讨

目的 检测冠心病(CHD)患者、血清淀粉样蛋白(SAA)及白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和超敏C-反应蛋白(hs-CRP)的变化,探讨其在CHD发病机制中的意义.方法 检测22例急性心肌梗死(AMI)、25例不稳定性心绞痛(UA)、30例稳定性心绞痛(SA)、30例健康者血清SAA、IL-6、TNF-α和hs-CRP水平.结果 CHD患者血清SAA、IL-6、TNF-α和hs-CRP水平均较对照组高(P＜0.01);并呈AMI＞ UA＞ SA的趋势(P＜0.05和0.01),且在冠脉单支病变、双支病变、三支病变者逐渐增高(P＜0.01);SAA与IL-6、TNF-α和hs-CRP水平显著相关(P＜0.01).结论 SAA、IL-6、TNF-α和hs-CRP可能参与了CHD的发病过程,可作为CHD病情观察的指标,以预防CHD急性冠脉事件的发生.     

超敏C-反应蛋白、MMP-3与TIMP-1在急性冠脉综合征的表达

目的探讨急性冠脉综合征(ACS)患者血清超敏C-反应蛋白(hs-CRP)质金属蛋白酶3、基(MMP-3)、金属蛋白酶组织抑制剂1(TIMP-1)与冠状动脉粥样硬化斑块稳定性的关系。方法对58例ACS患者,12例稳定型心绞痛患者及15例正常体检者外周血血清hs-CRP、MMP-3、TIMP-1水平进行检测并进行相关性分析。结果ACS组血清hs-CRP、MMP-3水平与正常对照组的差异具有显著性(P<0.05,P<0.01),急性心肌梗死组患者TIMP-1水平与稳定型心绞痛组、不稳定型心绞痛组、正常对照组的比较有非常显著性差异(P<0.01)。ACS组间指标相关分析显示,血清hs-CRP水平与MMP-3水平无相关性(r=0.099,P=0.539),与TIMP-1水平有显著相关性(r=0.415,P=0.007),血清MMP-3水平与TIMP-1水平有显著相关性(r=0.333,P=0.033)。结论ACS患者血清hs-CRP、MMP-3、TIMP-1水平升高与ACS的发生关联,提示与动脉粥样硬化(AS)斑块不稳定有关。