BACKGROUND:Heart failure (HF) is a leading cardiovascular disease worldwide. Jianxin Granule, a traditional Chinese medicine formula, has been clinically shown to improve cardiac function, yet its molecular mechanism remains unclear. Autophagy is crucial for maintaining cardiac homeostasis, and the mTOR pathway is a central negative regulator of autophagy. OBJECTIVES:To investigate whether Jianxin Granule confers cardioprotection in HF by modulating mTOR signaling to enhance autophagy and suppress apoptosis. Both in vivo and in vitro experiments were performed. METHODS:In male Sprague-Dawley rats HF model and in H9C2 cardiomyocytes exposed to H2O2, autophagy-related proteins and apoptotic markers were assessed by Western blotting and qRT-PCR. The specific role of mTOR signaling was further examined in cardiomyocytes transfected with mTOR-siRNA. RESULTS:Jianxin Granule markedly increased autophagic flux and reduced apoptosis in HF rats and these effects were attenuated by the autophagy inhibitor 3-methyladenine (3-MA). Consistent findings were observed in H2O2-injured H9C2 cells, where Jianxin Granule promoted autophagy and decreased apoptosis. In mTOR-siRNA-transfected cells, Jianxin Granule further enhanced autophagic flux and diminished apoptosis, supporting the involvement of mTOR signaling in its protective mechanism. CONCLUSION:Jianxin Granule protects against HF by regulating the mTOR pathway, thereby boosting autophagic flux and reducing cardiomyocyte apoptosis. These results provide mechanistic support for its clinical application in heart failure.

Diabetes mellitus (DM) is one of the most common chronic diseases worldwide, and diabetic cardiomyopathy (DCM) is one of the cardiovascular complications of DM, described as the development of abnormalities of myocardial structure/function associated with DM in the absence of coronary artery disease, hypertension, and valvular disease. The disease has an insidious onset and lacks effective treatment. Studies have shown that even with effective glycemic control, the progression of DCM cannot be prevented. Exploring the pathogenesis of DCM and identifying effective intervention targets is the focus and hotspot of current research. Silent message regulator 3 (Sirtuin3, SIRT3) is one of the members of the nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase family of sirtuins, and studies have confirmed that SIRT3 has a protective effect on cardiovascular disease and may become a new target for the treatment of cardiovascular diseases. Therefore, this paper emphasizes the role of SIRT3 in DCM, describes the mechanism of SIRT3 in DCM, and summarizes the methods to improve DCM by elevating the level of SIRT3, aiming to provide new perspectives for treating and delaying DCM.

Diabetic cardiomyopathy (DCM) is one of the cardiovascular complications of diabetes mellitus, which is different from myocardial damage caused by coronary ischemia, hypertension, and valvular disease. DCM lacks distinct clinical manifestations in its early stages, and current therapeutic approaches primarily focus on symptomatic management. Emerging evidence indicates that even with optimized glycemic regulation, the pathophysiological progression of DCM remains unmitigated. Exploring the pathogenic mechanism of DCM is the focus and hotspot of current research. Ferroptosis, an iron-dependent form of regulatory cell death, is crucial in DCM myocardial damage. Dysfunctional antioxidant defense system, increased oxidative stress, and elevated reactive oxygen species are the key mechanisms of ferroptosis in DCM. Thus, this review innovatively takes antioxidant proteins as the entry point, and for the first time systematically summarizes the molecular mechanism of antioxidant proteins to improve DCM by regulating the ferroptosis pathway, and summarizes the therapeutic strategy of medications to enhance ferroptosis in DCM by targeting the expression of antioxidant proteins, to explore the potential targets to improve ferroptosis in DCM, to provide a new perspective for the study of delaying the progression of DCM.

Jianxin Granules, a Traditional Chinese Medicine (TCM), consisting of eight flavors, including Huang Qi (astragalus), Hong Shen (red ginseng), Pu Huang (pollen typhae), Dan Shen (salvia miltiorrhiza), Zhu Ling (polyporus), Bai Zhu (atractylodes macrocephala), Gui Zhi (cassia twig), Ting Li Zi (semen lepidii). Jianxin granules has a multi-system, multi-target, and multi-directional comprehensive regulatory effect on inhibiting ventricular remodeling, which is an effective formulation for the prevention and treatment of heart failure, and has a good application prospect. However, many of the ingredients, including pharmacologically active ingredients, in the Jianxin granules remain unclear. Here, we attempted to develop a metabolomics method of component identification, quantitation, pattern recognition, and cross-comparison of Jianxin granules. Chemical analysis, component identification and quantification analyse of Jianxin granules were conducted with a combination of UHPLC-QTOF-MS/MS with bioinformatics. Assessment of the correlation between technical and bio-replicated pharmacological active ingredients was implemented by Principal Component Analysis (PCA), in addition to Partial Least Squares Discriminant Analysis (PLS-DA). UHPLC-QTOFMS/ MS, a metabolomics method, was developed and adapted to characterize Jianxin granules, which consisted of 178 to 216 molecular signatures. The quantitative analysis of 95 frequently occurring molecular signatures of Jianxin granules was carried out by a single exogenous reference internal standard. Of these, 47 have been identified using diverse databases, including 2 glycosylglycerol derivatives, 2 lipids, 2 spiro compounds, 2 cyclohexanecarboxylic acids, 2 glycosides, 5 terpenoids, 7 oligopeptides, 17 favonoids, and 8 various compounds, such as hydroxycoumarin, chalcone, benzofuran, benzodioxole, benzaldehyde, aromatic ketone, and alkyl cafeate ester. The established method demonstrates robust reliability and reproducibility, making it suitable for various applications including compositional identification, quantification, and quality assessment of the pharmacologically active constituents in Jianxin granules.

BACKGROUND: Jianxin (JX) granules is a traditional Chinese medicine widely used in the treatment of heart failure (HF), but the mechanism is unclear. This study aimed to investigate the mechanism of JX granules in the treatment of HF based on network pharmacology analysis and in-vivo experiments. METHODS: A series of network pharmacology methods was employed to ascertain potential targets and critical pathways implicated in the therapeutic action of JX granules against HF. Subsequently, molecular docking was utilized to investigate the binding affinity of key active constituents within JX granules to these targets. In-vivo experiments, echocardiography, hematoxylin and eosin, Masson's trichrome assay, and western blot analysis were conducted to validate the efficacy and mechanism of JX granules in treating rats with HF. RESULTS: A total of 122 active components, 896 drug targets, 1216 HF-related targets, and 136 targets pertinent to drug-disease interactions were identified. 151 key targets and 725 core clusters were detected through protein-protein interaction network analysis. Among these, interleukin 6 (IL -6), vascular endothelial growth factor a (VEGFA), and serine/ threonine kinase 1 (AKT1) were core hub genes. Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis revealed the critical pathways, including epidermal growth factor receptor (EGFR), advanced glycation end products (AGEs) and their receptors (RAGE) pathway, along with hypoxia-inducible factor 1 (HIF-1) signaling pathway. Molecular docking studies demonstrated high binding affinities between key targets and the pivotal active ingredients of Danshenol A, salvianolic acid B, and arachidonic acid. Furthermore, animal studies corroborated that JX granules improve cardiac function and reduce myocardial fibrosis, potentially by modulating the expression of IL -6, VEGFA, and p-AKT1. CONCLUSIONS: The bioactive components within JX granules, such as Danshenol A, salvianolic acid B, and arachidonic acid may exert therapeutic effects on HF through modulation of IL -6, VEGFA, and AKT1 gene expression. This study provides a scientific basis for subsequent clinical application of JX granules and an in-depth investigation of their mechanisms of action.

目的 从NLRP3/Caspase-1/GSDMD信号通路探讨健心颗粒对糖尿病心肌病大鼠心肌焦亡的影响,明确其作用机制.方法 将40只6周龄SPF级SD大鼠按随机数字表法分成空白组、模型组、西药组、中药组及西药+中药组,每组8只.空白组不予造模,其余各组采用高糖高脂喂养+腹腔注射链脲佐菌素的方法 制备糖尿病心肌病模型.造模成功后空白组、模型组均给予生理盐水5 mL,西药组给予卡托普利5 mg/kg,中药组给予健心颗粒3.2 g/kg,西药+中药组予健心颗粒3.2 g/kg+卡托普利5 mg/kg,早晚各灌胃1次,共8周.心脏彩超比较5组大鼠心脏室间隔厚度(IVST)、左心室射血分数(LVEF)、左室舒张末径(LVEDD)、左室收缩末径(LVESD)情况;TUNEL法检测5组大鼠心肌细胞焦亡情况;qPCR及Western blot分别检测5组大鼠心肌组织NOD样受体热蛋白结构域3(NLRP3)、半胱氨酸蛋白酶-1(Caspase-1)、消皮素D(GSDMD)mRNA表达水平及蛋白表达量;ELISA法检测5组大鼠血清白细胞介素-1β(IL-1β)、白细胞介素-18(IL-18)含量.结果 与空白组比较,模型组IVST、LVEF降低,LVEDD、LVESD升高,心肌细胞焦亡增多,NLRP3、Caspase-1、GSDMD mRNA表达水平及蛋白表达量均上升,血清中的IL-1β、IL-18含量显著增多(P＜0.05);与模型组比较,各给药组IVST、LVEF明显升高,LVEDD、LVESD降低,心肌细胞焦亡减少,NLRP3、Caspase-1、GSDMD mRNA表达水平及蛋白表达量均下降,血清中的IL-1β、IL-18含量减少(P＜0.05);其中,西药+中药组上述指标改善最显著,而中药组与西药组组间差异无统计学意义(P＞0.05).结论 健心颗粒可能通过调控NLRP3/Caspase-1/GSDMD信号通路,抑制DCM大鼠心肌细胞焦亡.

目的 采用检测肌钙蛋白(cTnI)和左室整体长轴峰值应变(GLS)定量评价健心颗粒防治乳腺癌患者蒽环类药物所致亚临床心脏毒性的可行性.方法 选取2015年1月至2020年12月在本院确诊的乳腺癌患者30例,随机分为治疗组和对照组.对照组为规范化蒽环类药物化疗方案(含阿霉素或表柔比星、吡柔比星);治疗组在此基础上加用健心颗粒10g,每日3次口服.分别于化疗前1天及化疗两周期后的第1天,观察临床症状,检查心电图,检测cTnI、肌酸激酶同功酶(CK-MB)、N端脑钠肽前体(NT-proBNP)、超氧化物歧化酶(SOD)、丙二醛(MDA);常规超声心动图分析E/e'、E/A、左室射血分数(EF)、左室缩短分数(FS)、斑点追踪显像分析GLS.结果 化疗后,治疗组临床症状改善,心电图异常的发生率减低,cTnI、CK-MB、NT-proBNP、MDA均低于对照组,而SOD、GLS高于对照组,两组差异有统计学意义(P＜0.05);但两组间E/e'、E/A、EF、FS的变化差异无统计学意义(P＞0.05).结论 cTnI和GLS在评估蒽环类药物早期心肌损伤及药物干预效果方面具有重要价值,健心颗粒可改善乳腺癌蒽环类化疗所致的亚临床心脏毒性.

目的 观察并分析小青龙汤加减方穴位贴敷治疗慢性心力衰竭阳虚水泛证的临床疗效及其安全性.方法 本研究对象为60例慢性心力衰竭阳虚水泛证患者,随机分成治疗组和对照组,两组病例数均为30例,均给予西医综合治疗,治疗组另加小青龙汤加减方穴位贴敷治疗,治疗10d后,观察并比较两组临床疗效及不良反应情况.结果 治疗后,治疗组总有效率为80.00％;对照组总有效率为66.67％,两组对比有统计学差异(P＜0.05);经治疗,两组血浆BNP水平较治疗前明显降低(P＜0.05),治疗组优于对照组(P＜0.05);两组6MWD较治疗前明显增加(P＜0.05),治疗组优于对照组(P＜0.05).结论 小青龙汤加减方穴位贴敷治疗慢性心力衰竭阳虚水泛证疗效肯定,且安全性高,值得临床借鉴使用.

目的 采用二维斑点追踪技术评价健心颗粒对糖尿病心肌病(DCM)患者心室功能的影响.方法 选择2017年1月至2019年12月于本院心血管内科新确诊的80名DCM患者为研究对象,分为观察组和对照组,每组40例,两组均给予常规西药治疗方案,观察组在此基础上给予健心颗粒,两组疗程为1个月.比较两组患者在治疗前后临床症状、收缩压、舒张压、左室收缩期整体长轴峰值应变、整体圆周峰值应变、左室射血分数、NT-proBNP等指标变化情况.结果 观察组临床疗效总有效率(85.0％)明显高于对照组(60.0％).治疗后,两组空腹血糖及NT-proBNP均显著减低,但观察组NT-proBNP、射血分数、左室收缩期整体长轴(圆周、径向)峰值应变改善情况明显大于对照组.两组间LA、LVDd、IVSd、LVPWd、E/A治疗前后差异无统计学意义(P＞0.05).结论 健心颗粒在改善DCM左室结构前,已明显改善其心室功能;二维斑点追踪技术能够早期准确地对治疗效果进行评价,值得临床推广及应用.

目的 探讨疏肝活血方柴胡疏肝散加减治疗心肌桥的有效性和安全性.方法 选取2014年10月-2016年2月收治住院的患者,经冠状动脉造影术检查诊断为心肌桥,并符合中医气滞血瘀型症候的研究对象,共60例.随机分为对照组和治疗组,对照组30例采取常规用药美托洛尔缓释片23.75～47.5 mg每日1次(有β-受体阻滞剂禁忌症者改用维拉帕米缓释片0.24 g每日1次).治疗组30例予柴胡疏肝散加减.治疗观察6周后比较2组治疗效果及药物不良反应.结果 治疗组的中医证候积分、心电图疗效、心绞痛临床症状改善均优于对照组常规西药治疗,并且观察过程中未见不良反应.结论 柴胡疏肝散加减治疗气滞血瘀型心肌桥临床效果明显,能够有效改善患者症状,安全性可靠.

目的 分析探究中西医结合治疗心肾阳虚型慢性心力衰竭的临床效果.方法 选择100例心肾阳虚型慢性心力衰竭患者纳入研究,将其随机分为两组.其中对照组患者给予常规西医治疗方案,观察组患者接受中西医结合治疗,对比分析两组的临床治疗效果.结果 观察组患者的治愈率以及总有效率均显著高于对照组(P＜0.05),同时观察组患者的住院时间显著短于对照组(P＜0.05).结论 中西医结合治疗心肾阳虚型慢性心力衰竭的临床效果突出,可以有效强化患者的临床治疗效果,具有较大的临床应用价值.

中药中毒事件的相继报道,使得中药安全性的问题在社会上引起了不少关注.正确认识中药毒性,了解其毒性的相对性,对其毒性原因进行综合分析,如选用药物品种不正确、炮制不当、药物不对症、配伍不合理、使用剂量和疗程过大过长、忽略个体差异等,并制定相应的应对策略,在选用正确品种药物并进行规范炮制的基础上,对不同体质、不同疾病表现的患者进行辨证施治,予以适当剂量的药物,进行合理配伍,并严格遵守药物特殊煎煮方法,中病即止,勿过量服用等.从上述这些方面着手,从而掌握药物的毒性,使其更好地运用于临床疾病的治疗.

Apelin plays important roles in cardiovascular homeostasis. However, its effects on the mechanoenergetics of heart failure (HF) are unavailable. We attempted to investigate the effects of apelin on the left ventricular-arterial coupling (VAC) and mechanical efficiency in rats with HF. HF was induced in rats by the ligation of the left coronary artery. The ischemic HF rats were treated with apelin or saline for 12 weeks. The sham-operated animals served as the control. The left ventricular (LV) afterload and the systolic and diastolic functions, as well as the mechanoenergetic indices were estimated from the pressure-volume loops. Myocardial fibrosis by Masson’s trichrome staining, myocardial apoptosis by TUNEL, and collagen content in the aorta as well as media area in the aorta and the mesenteric arteries were determined. Our data indicated that HF rats manifested an increased arterial load (Ea), a declined systolic function (reduced ejection fraction, +dP/dtmax, end-systolic elastance, and stroke work), an abnormal diastolic function (elevated end-diastolic pressure, τ, and declined −dP/dtmax), and decreased mechanical efficiency. Apelin treatment improved those indices. Concomitantly, increased fibrosis in the LV myocardium and the aorta and enhanced apoptosis in the LV were partially restored by apelin treatment. A declined wall-to-lumen ratio in the mesenteric arteries of the untreated HF rats was further reduced in the apelin-treated group. We concluded that the rats with ischemic HF were characterized by deteriorated LV mechanoenergetics. Apelin improved mechanical efficiency, at least in part, due to the inhibiting cardiac fibrosis and apoptosis in the LV myocardium, reducing collagen deposition in the aorta and dilating the resistant artery.

Background Soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) may be a potential biomarker of coronary artery disease (CAD) and stroke. Objective We aimed to investigate the association and prognostic value of elevated sLOX-1 concentrations with regard to long-term major adverse cardiovascular and cerebrovascular events (MACCEs) in patients with CAD undergoing primary percutaneous coronary intervention (PCI). Methods A total of 1011 patients were enrolled. Serum sLOX-1 concentrations were detected by the enzyme-linked immunosorbent assay (ELISA). Patients were followed for 2 years. Multivariate Cox regression and Kaplan-Meier survival curve were explored to assess the association between sLOX-1 and MACCEs. A receiver operating characteristic (ROC) curve was used to evaluate the diagnostic efficacy of sLOX-1. Results Two-year MACCEs were associated with serum sLOX-1 concentrations (HR 1.278, 95% CI 1.019-1.604, P = 0.034), left main disease (HR 2.938, 95% CI 1.246-6.925, P = 0.014), small-caliber stents used (HR 2.207, 95% CI 1.189-4.095, P = 0.012), and total stent length (HR 1.057, 95% CI 1.005-1.112, P = 0.030). Serum sLOX-1 concentration ≥ 1.10 ng/ml had maximum sensitivity and specificity in predicting the occurrence of 2-year MACCEs (P < 0.001). Patients with higher serum sLOX-1 concentrations showed a significantly higher incidence of MACCEs in the Kaplan-Meier curve (P < 0.001). The combination of any of the risk factors identified in multiple Cox regression was associated with a stepwise increase in MACCE rate (P < 0.001). Conclusions High baseline serum sLOX-1 concentration predicts 2-year MACCEs and shows an additional prognostic value to conventional risk factors in patients after primary PCI. sLOX-1 determination might play a complementary role in the risk stratification of patients with CAD treated with PCI.

INTRODUCTION:Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in the pathophysiology of atherosclerosis and acute coronary syndromes (ACS). Circulating soluble LOX-1 (sLOX-1) has been linked to the risk of coronary artery disease (CAD). Our aim was to test if baseline serum sLOX-1 was associated with major adverse cardiovascular events (MACE) in patients with stable CAD.MATERIALS AND METHODS:This multicentre pilot study enrolled 833 stable CAD patients. All patients were followed for two years. Serum sLOX-1 concentrations were detected by enzyme-linked immunosorbent assay (ELISA). The association between sLOX-1 concentrations and MACE was assessed by logistic regression, Kaplan-Meier survival curves and Cox proportional hazards analyses. Logistic regression analysis was employed to assess the predictors of complex lesion.RESULTS:Multivariate logistic regression analysis revealed that sLOX-1 concentration was an independent predictor of MACE (OR 2.07, 95%CI 1.52 - 2.82; P < 0.001). Kaplan-Meier cumulative survival curves showed that the incidence of MACE in patients with a high sLOX-1 concentration was significantly higher than in patients with an intermediate or low sLOX-1 concentration (P < 0.001). Soluble LOX-1 concentrations were independently correlated with coronary complex lesions (OR 2.32, 95%CI 1.81 - 2.97; P < 0.001).CONCLUSIONS:Baseline sLOX-1 concentrations were correlated with 2-year MACE in stable CAD patients. Furthermore, patients with high serum sLOX-1 concentrations had higher cumulative incidence of MACE compared to those with low serum sLOX-1 concentrations.

Objective To observe the effect of Kangxin Decoction on the cell apoptosis in a rat model of ischemic cardiomyopathy(ICM),and to explore the underlying mechanisms,including its effects on the expression of PI3K/Akt/FoxO1 signaling pathway.Methods Sixty-six rats were randomly divided into six groups:the sham group,the model group,the Captopril group,the low dose Kangxin Decoction group,the middle dose Kangxin Decoction group,and the high dose Kangxin Decoction group,11 in each group.The model rat was established by ligating the left anterior descending artery(LAD).Captopril at 2.86 mg · kg-1 · d-1,and Kangxin Decoction at 9.2,18.4,and 36.8 g · kg-1 · d-1 were administered to rats in the Captopril group and three Kangxin Decoction groups by gastrogavage,respectively.All the medication was performed twice daily and continued for two weeks.The model group was fed with the same volume of saline (10 mL · kg-1 · d-1).Cell apoptosis was observed by TUNEL,the expressions of Bcl-2,Bax,Caspase-3,PI3K,Akt and FoxO1 protein were detected by Western blot,and PI3K,Akt,FoxO1 mRNA detected by RT-PCR.Results Compared with the sham group,cardiomyocytes apoptosis was significantly increased in model group (P ＜0.05),the expression of Bax and Caspase-3 protein were remarkably upregulated (P ＜0.05,P ＜ 0.01) while Bcl-2 down-regulated (P ＜0.01);the expression of PI3K,p-Akt,pFoxO1 protein and PI3K,Akt,FoxO1 mRNA were all remarkably down-regulated (all P ＜0.05).Compared with the model group,cardiomyocytes apoptosis was significantly reduced in three Kangxin Decoction groups and Captopril group (all P ＜0.01),the expression of Bax and Caspase-3 protein were remarkably down-regulated while Bcl-2 up-regulated (all P ＜0.05);the expression of PI3K,p-Akt,p-FoxO1 protein and PI3K,Akt,FoxO1 mRNA were all remarkably up-regulated (all P ＜0.01).Such effects were more significant in high dose Kangxin Decoction group and Captopril group than in low or middle dose Kangxin Decoc tion group (all P ＜0.05).Conclusion Kangxin Decoction could reduce cardiomyocyte apoptosis in ICM rats,which may be the results of its activating of PI3K/Akt/FoxO1 signaling pathway.

目的 探索经皮血管球囊成形术联合支架植入术对2型糖尿病足病的效果.方法 选取2015年4月-2017年4月期间该院2型糖尿病足病100例患者,抽签化分组,即50例/组,对照组和观察组分别采用传统手术治疗和经皮血管球囊成形术联合支架植入术治疗.结果 观察组患者的足底动脉的血流最大速度(13.58±1.58)cm/s、胫前动脉的血流最大速度(26.78±1.63)cm/s、腓动脉的血流最大速度(20.48±1.86)cm/s、6 min行走距离(554.74±56.86)m、踝肱指数(0.87±0.76)、并发症发生率(2.00％)均优于对照组(P＜0.05).结论 对2型糖尿病足病患者实施经皮血管球囊成形术联合支架植入术治疗效果显著,且安全性较高.

目的 初步观察中医优化诊疗不稳定性心绞痛的临床疗效和安全性,为进一步进行卫生经济学评估提供临床依据.方法 选择本院门诊及住院的不稳定心绞痛患者300例,采用随机数字表法随机分为两组,对照组给予西医常规药物治疗,治疗组在对照组治疗基础上根据辨证分型,分别给予协定处方畅脉饮、化痰活血方、心脉2号;两组均以治疗30天为一疗程.结果 治疗组心绞痛疗效、心电图疗效、心血管事件的发生率,中医证候积分及治疗前后积分差值比较等均较对照组优(P均<0.05).结论 中医优化治疗不稳定性心绞痛疗效确切.

目的:观察康心饮对缺血性心肌病(ischemic cardiomyopathy,ICM)大鼠基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)及基质金属蛋白酶抑制剂-2(TIMP-2)的影响,探讨其对慢性心肌缺血的作用及可能机制.方法:制备ICM大鼠模型,造模成功后随机分为假手术组、模型组、卡托普利组和康心饮组,HE染色和Masson染色及免疫组化法检测MMP-2、MMP-9及TIMP-2的表达.结果:HE染色显示,与模型组比较,康心饮组心肌细胞排列比较规则,细胞坏死、变性水肿、炎性细胞浸润明显减少;Masson染色显示,康心饮组胶原纤维明显比模型组减少;免疫组化显示,与模型组比较,康心饮组MMP-2、MMP-9表达有显著减少(P＜0.01),TIMP-2表达显著增多(P＜0.05),与卡托普利组相似.结论:康心饮能改善ICM大鼠心肌纤维化,其机制可能是下调MMP-2、MMP-9和上调TIMP-2的表达.