Roles and mechanisms of puerarin on cardiovascular disease：A review.

Cardiovascular diseases (CVDs) are now the leading cause of mortality and morbidity worldwide，resulting in a large global economic burden. Recently, complementary and alternative medicine, such as traditional Chinese medicine (TCM) have received great attention. Puerarin (Pue) is an isoflavone isolated from the roots of Pueraria lobata (Willd.) Ohwi (also named "Ge gen" in China), and is a versatile TCM herb used for the treatment of fever, diarrhea, diabetes mellitus CVDs and cerebrovascular diseases. Numerous lines ofin vitro studies, as well as in vivo animal experiments have established that Pue offers beneficial roles against the progression of atherosclerosis, ischemic heart diseases, heart failure hypertension and arrhythmia by inhibiting pathological processes, such as the mitigation of endothelium injury, protection against inflammation, the disturbance of lipid metabolism, protection against ischemic reperfusion injury, anti-myocardial remodeling and other effects. Here, we provide a systematic overview of the pharmacological actions and molecular targets of Pue in cardiovascular disease prevention and treatment, to provide insights into the therapeutic potential of Pue in treating cardiovascular diseases.

Huoxin pill prevents acute myocardial ischaemia injury via inhibition of Wnt/ß-catenin signaling.

Myocardial infarction (MI) is one of the leading causes of death worldwide, and due to the widespread and irreversible damage caused, new therapeutic treatments are urgently needed in order to limit the degree of ischaemic damage following MI. Aberrant activation of Wnt/ß-catenin signalling pathway often occurs during cardiovascular diseases including MI, which results in excess production of reactive oxygen species (ROS) and further promotes myocardial dysfunction. Huoxin pill (HXP) is a Traditional Chinese Medicine formula that has been widely used in the treatment of coronary heart disease and angina; however, its mechanisms remain unclear. Here, we performed mouse models of MI and examined the effects and mechanisms of HXP in protecting against MI-induced ischaemic damage. Our study showed that administration with HXP robustly protected against MI-induced cardiac injuries, decreased infarct size and improved cardiac function. Moreover, HXP attenuated ischaemia-induced DNA damage occurrence in vivo and H2 O2 -induced DNA damage occurrence in vitro, via potent inhibition of adverse Wnt/ß-catenin signalling activation. Our study thus elucidated the role and mechanism of HXP in protecting against MI and oxidative stress-induced injuries and suggests new therapeutic strategies in ischaemic heart disease via inhibition of Wnt/ß-catenin signalling pathway.

Pachymic Acid Attenuated Doxorubicin-Induced Heart Failure by Suppressing miR-24 and Preserving Cardiac Junctophilin-2 in Rats.

Defects in cardiac contractility and heart failure (HF) are common following doxorubicin (DOX) administration. Different miRs play a role in HF, and their targeting was suggested as a promising therapy. We aimed to target miR-24, a suppressor upstream of junctophilin-2 (JP-2), which is required to affix the sarcoplasmic reticulum to T-tubules, and hence the release of Ca2+ in excitation-contraction coupling using pachymic acid (PA) and/or losartan (LN). HF was induced with DOX (3.5 mg/kg, i.p., six doses, twice weekly) in 24 rats. PA and LN (10 mg/kg, daily) were administered orally for four weeks starting the next day of the last DOX dose. Echocardiography, left ventricle (LV) biochemical and histological assessment and electron microscopy were conducted. DOX increased serum BNP, HW/TL, HW/BW, mitochondrial number/size and LV expression of miR-24 but decreased EF, cardiomyocyte fiber diameter, LV content of JP-2 and ryanodine receptors-2 (RyR2). Treatment with either PA or LN reversed these changes. Combined PA + LN attained better results than monotherapies. In conclusion, HF progression following DOX administration can be prevented or even delayed by targeting miR-24 and its downstream JP-2. Our results, therefore, suggest the possibility of using PA alone or as an adjuvant therapy with LN to attain better management of HF patients, especially those who developed tolerance toward LN.

Effects of Danhong injection on cardiac function and blood lipid in patients with angina pectoris of coronary heart disease: A protocol for randomized, double-blind, placebo-controlled clinical trial.

BACKGROUND: Angina pectoris of coronary heart disease is the leading cause of death worldwide. Danhong injection is a supplement for angina pectoris of coronary heart disease. A large number of studies have confirmed its efficacy and safety. However, there is no rigorous clinical study to evaluate the effects of Danhong injection on cardiac function and blood lipid in patients with angina pectoris of coronary heart disease. METHODS: This is a prospective, randomized, double-blind, placebo-controlled trial to study the effects of Danhong injection on cardiac function and lipid profile in patients with angina pectoris of coronary heart disease. Participants will be randomly divided into treatment group and control group. The treatment group will be treated with Danhong injection and the control group will be treated with placebo under basic treatment according to recommended guideline, and followed up for 3 months after 14 consecutive days of treatment. Outcomes include: cardiac function (left ventricular end-diastolic diameter); left ventricular end-systolic diameter; left ventricular ejection fraction, blood lipid levels (total cholesterol; triacylglycerol; low density lipoprotein cholesterol; high density lipoprotein cholesterol), the number of angina attacks per week, total amount of nitroglycerin tablets, and adverse reactions. DISCUSSION: This study will evaluate the efficacy of Danhong injection in improving cardiac function and blood lipid in patients with angina pectoris of coronary heart disease. The results of this study will provide reference for clinical use of Danhong injection to improve cardiac function and blood lipid in patients with angina pectoris of coronary heart disease.Trial registration: OSF Registration number: DOI 10.17605/OSF.IO/TPZJ5.

A randomized controlled protocol on the effect of moxibustion on the cardiac function and quality of life in patients with chronic heart failure.

BACKGROUND: Chronic heart failure (CHF) is the final result of various cardiovascular diseases, with high morbidity and high mortality, which seriously threaten people's health and quality of life. It has become a public health problem in the world. There is currently no specific treatment. Moxibustion, as a complementary and replacement therapy, has advantages in the treatment of chronic heart failure, but it lacks standard clinical studies to verify it. Therefore, the purpose of this randomized controlled trial is to evaluate the effect of moxibustion on the heart function and quality of life of patients with CHF. METHODS: This is a prospective randomized controlled trial to study the effect of moxibustion on the heart function and quality of life of patients with CHF. This is approved by the clinical research ethics committee of our hospital. Patients were randomly divided into observation group (moxibustion combined with Western medicine treatment group) or control group (conventional Western medicine treatment group). There is a follow-up for 3 months after 6 weeks of treatment. Observation indicators include total effective rate of cardiac function improvement, Minnesota Living with Heart Failure Questionnaire , left ventricular ejection fraction , N-terminal pro-brain natriuretic peptide , 6-minute walk test , adverse reactions, etc. Data were analyzed using the statistical software package SPSS version 18.0 (Chicago, IL). DISCUSSION: This study will evaluate the clinical efficacy of moxibustion in the treatment of CHF. The results of this study will provide a reliable reference for the clinical choice of moxibustion as an adjuvant treatment for chronic heart failure. TRIAL REGISTRATION: OSF Registration number: DOI 10.17605/OSF.IO/29XE7.

ω-3 fatty acid alleviates virus-induced myocardial injury by regulating TLR4 and TLR3 expression.

The specific pathogenesis of viral-induced myocardial injury is unclear. TLR regulation plays an important role in virus-induced myocardial injury. The therapeutic effect and possible mechanism of omega-3 fatty acids in patients with viral-induced myocardial injury must be investigated. The study population was randomly divided into three groups: a healthy control group (n = 50); general treatment group (n = 40); and general treatment with ω-3 polyunsaturated fatty acid group (n = 36). We detected the mRNA levels of TLR3 and TLR4, downstream signal pathway proteins, inflammatory factors, oxidative stress markers, and myocardial enzymes in patients and healthy controls. ω-3 fatty acid therapy in patients with virus-induced myocardial injury significantly regulates the expression of TLR3 and TLR4 and their downstream signal protein, increases antioxidant expression, reduces the secretion of inflammatory factors, alleviates myocardial injury, and improves cardiac function. This provides a new strategy to treat virus-induced myocardial injury.

Calycosin attenuates doxorubicin-induced cardiotoxicity via autophagy regulation in zebrafish models.

Anthracyclines are highly effective chemotherapeutics for antineoplastic treatment. However, cumulative cardiotoxicity is the main side effect with poor prognosis. No mechanism-based therapy is currently available to reverse chronic anthracycline-induced cardiotoxicity (AIC) after the deterioration of cardiac function. Calycosin (CA) is the main compound extracted from the traditional Chinese medicine Astragalus, and it has diverse beneficial effects, including autophagy modulation, anti-inflammatory and anti-tumor effects. Autophagy dysregulation is an important pathological event in AIC. Our study demonstrated a cardioprotective effect of CA in a zebrafish embryonic AIC model. To assess the effect of CA on late-onset chronic AIC, adult zebrafish were treated with CA 28 days after doxorubicin (DOX) injection, at which point heart function was obviously impaired. The results demonstrated that DOX blocked autophagic activity in adult zebrafish 8 weeks post-injection, and CA treatment improved heart function and restored autophagy. Further in vitro experiments demonstrated that atg7, which encodes an E1-like activating enzyme, may play an essential role in the CA regulation of autophagy. In conclusion, we used a rapid pharmacological screening system in embryo-adult zebrafish in vivo and elucidated the mechanism of gene targeting in vitro.

The impact of chicory (Cichoriumintybus L.) on hemodynamic functions and oxidative stress in cardiac toxicity induced by lead oxide nanoparticles in male rats.

BACKGROUND: A common environmental pollutant, lead can induce toxicity in several organ systems. A range of industrial and/or household materials and products contain lead, and food/liquid ingestion and inhalation are the mechanisms through which lead is introduced into the human body. OBJECTIVE: Since knowledge about the cardiac toxicity of acute lead nanoparticles is limited, this work sought to shed more light on the issue by investigating the therapeutic effects of chicory extract based on rat models to elevate cardiac functions and oxidative stress. METHODS: Four research groups were used, each consisting of ten albino rats of male sex and adult age. The groups were: control group, chicory group, lead oxide nanoparticle group, and lead oxide nanoparticle + chicory group. RESULTS: Compared to the control and chicory groups, the lead oxide nanoparticle group displayed a notable increase in heart functions and oxidative stress markers as well as alterations in cardiac histological structure. On the other hand, cardiac function modifications were counteracted through four-week administration of lead oxide nanoparticles alongside chicory. CONCLUSION: Heart damage caused by lead oxide nanoparticles may be attenuated by chicory through scavenging of free radicals.

A retrospective study on the short-term effect of high-dose spironolactone (80 mg/d) on chronic congestive heart failure.

ABSTRACT: To explore the short-term effect of high-dose spironolactone (80 mg/d) on chronic congestive heart failure (CHF).The general clinical data of 211 patients with CHF from February 2016 to August 2019 were collected and analyzed. Patients were divided into Low-dose group (taking 40 mg/d spironolactone) and High-dose group (taking 80 mg/d spironolactone) according to the patient's previous dose of spironolactone. The changes of B-type brain natriuretic peptide (BNP), NT-pro BNP (N terminal pro B type natriuretic peptide), echocardiography, 6-minute walking test (6MWT), and comprehensive cardiac function assessment data were collected for analysis.Compared with before treatment, the blood potassium of the two groups increased significantly (P < .05), but the blood potassium did not exceed the normal range. Compared with before treatment, BNP, NT-pro BNP, LVEDD, LVEDV and NYHA grading were significantly decreased (P < .05), LVEF and 6-MWT were significantly increased (P < .05). Compared with the Low-dose group, the high-dose group BNP (117.49 ±â€Š50.32 vs 195.76 ±â€Š64.62, P < .05), NT-pro BNP (312.47 ±â€Š86.28 vs 578.47 ±â€Š76.73, P < .05), LVEDD (45.57 ±â€Š5.69 vs 51.96 ±â€Š5.41, P <.05), LVEDV (141.63 ±â€Š51.14 vs 189.85 ±â€Š62.49, P < .05) and NYHA grading (1.29 ±â€Š0.41 vs 1.57 ±â€Š0.49, P < .05) were significantly reduced, but, 6-MWT (386.57 ±â€Š69.72 vs 341.73 ±â€Š78.62, P < .05), LVEF (41.62 ±â€Š2.76 vs 36.02 ±â€Š2.18, P < .05) and total effective rate (92.68% vs 81.39%, P < .05) increased significantly.Compared with 40 mg spironolactone, 80 mg spironolactone can rapidly reduce BNP and NT-pro BNP concentration, enhance exercise tolerance, improve clinical signs and cardiac function classification, and has better efficacy.

Garlic Derived Diallyl Trisulfide in Experimental Metabolic Syndrome: Metabolic Effects and Cardioprotective Role.

This study aimed to examine the effects of diallyl trisulfide (DATS), the most potent polysulfide derived from garlic, on metabolic syndrome and myocardial function in rats with metabolic syndrome (MetS). For that purpose, we used 36 male Wistar albino rats divided into control rats, rats with MetS and MetS rats treated with 40 mg/kg of DATS every second day for 3 weeks. In the first part, we studied the impact of DATS on MetS control and found that DATS significantly raised H2S, decreased homocysteine and glucose levels and enhanced lipid and antioxidative, while reducing prooxidative parameters. Additionally, this polysulfide improved cardiac function. In the second part, we investigated the impact of DATS on ex vivo induced ischemia/reperfusion (I/R) heart injury and found that DATS consumption significantly improved cardiodynamic parameters and prevented oxidative and histo-architectural variation in the heart. In addition, DATS significantly increased relative gene expression of eNOS, SOD-1 and -2, Bcl-2 and decreased relative gene expression of NF-κB, IL-17A, Bax, and caspases-3 and -9. Taken together, the data show that DATS can effectively mitigate MetS and have protective effects against ex vivo induced myocardial I/R injury in MetS rat.

Latifolin protects against myocardial infarction by alleviating myocardial inflammatory via the HIF-1α/NF-κB/IL-6 pathway.

CONTEXT: The Traditional Chinese herb medicine Dalbergia odorifera T. Chen (Fabaceae), exerted a protective effect on myocardial ischaemia. Latifolin is a neoflavonoid extracted from Dalbergia odorifera. It has been reported to have the effects of anti-inflammation and cardiomyocyte protection. OBJECTIVE: To investigate whether latifolin can improve myocardial infarction (MI) through attenuating myocardial inflammatory and to explore its possible mechanisms. MATERIALS AND METHODS: Left coronary artery was ligated to induce a rat model of MI, and the rats were treated with sodium carboxymethyl cellulose (CMC-Na) or different doses of latifolin (25, 50, 100 mg/kg/d) by oral gavage for 28 days. Serum contents of myocardial enzyme were measured at seven and fourteen days after treatment. Cardiac function, infarct size, histopathological changes and inflammatory cells infiltration was assessed at 28 days after treatment. Western blotting was used to investigate the underlying mechanisms. RESULTS: Latifolin treatment markedly decreased the contents of myocardial enzymes, and increased left ventricular ejection fraction (85.27% vs. 59.11%) and left ventricular fractional shortening (62.71% vs. 45.53%). Latifolin was found to significantly reduced infarction size (27.78% vs. 39.07%), myocardial fibrosis and the numbers of macrophage infiltration (436 cells/mm2 vs. 690 cells/mm2). In addition, latifolin down-regulated the expression levels of hypoxia-inducible factor-1α (0.95-fold), phospho-nuclear factor-κB (0.2-fold) and interleukin-6 (1.11-fold). DISCUSSION AND CONCLUSIONS: Latifolin can protect against myocardial infarction by improving myocardial inflammation through the HIF-1α/NF-κB/IL-6 signalling pathway. Accordingly, latifolin may be a promising drug for pharmacological treatment of ischaemic cardiovascular disease.

Ethanol Extract of Chinese Hawthorn (Crataegus pinnatifida) Fruit Reduces Inflammation and Oxidative Stress in Rats with Doxorubicin-Induced Chronic Heart Failure.

BACKGROUND Chinese hawthorn (Crataegus pinnatifida) fruit is a traditional Chinese medicine for treatment of digestive system and cardiovascular diseases. The fruit contains polyphenol compounds, such as epicatechin, that have anti-inflammatory activity. This study aimed to investigate the effects of an alcohol extract of hawthorn fruit (HAE) on inflammation and oxidative stress in rats with doxorubicin-induced chronic heart failure (CHF). MATERIAL AND METHODS Rats were intraperitoneally injected with doxorubicin to induce CHF and subsequently treated with HAE intragastrically once daily for 6 weeks. At the end of the experiment, echocardiographic and hemodynamic parameters were assessed, and enzyme-linked immunoassays were used to detect the levels of cardiac injury markers (brain natriuretic peptide, creatine kinase-MB, aspartate aminotransferase, lactate dehydrogenase, copeptin, and adrenomedullin), oxidative stress markers (glutathione peroxidase and malondialdehyde), and inflammatory cytokines (interleukin [IL]-6, IL-8, IL-1ß, and tumor necrosis factor-a). The IL-1ß, IL-6, glutathione peroxidase-1, and catalase mRNA levels were also measured by quantitative real-time polymerase chain reaction. RESULTS Our findings indicated that HAE exerts a cardioprotective effect, as shown by improved echocardiographic and hemodynamic parameters, decreased activity of serum myocardial enzymes, reduced serum levels of CHF markers, and inhibited inflammatory response in cardiac tissue. In addition, HAE treatment downregulated the mRNA expression of IL-1ß and tumor necrosis factor-alpha and upregulated the mRNA expression of glutathione peroxidase-1 and catalase compared with untreated doxorubicin-induced CHF rats. CONCLUSIONS HAE shows promise for the prevention and treatment of CHF. The cardioprotective effect of HAE appears to be related to inhibition of both the inflammatory response and oxidative stress in vivo.

Early Noninvasive Cardiac Testing After Emergency Department Evaluation for Suspected Acute Coronary Syndrome.

Importance: Professional guidelines recommend noninvasive cardiac testing (NIT) within 72 hours of an emergency department (ED) evaluation for suspected acute coronary syndrome. However, there is inexact evidence that this strategy reduces the risk of future death or acute myocardial infarction (MI). Objective: To evaluate the effectiveness of early NIT in reducing the risk of death or acute MI within 30 days. Design, Setting, and Participants: This retrospective, multicenter cohort study within the Kaiser Permanente Southern California integrated health care delivery system compared the effectiveness of early noninvasive cardiac testing vs no testing in patients with chest pain and in whom acute MI was ruled out who presented to an ED from January 2015 to December 2017. Patients were followed up for up to 30 days after emergency department discharge. Exposures: Noninvasive cardiac testing performed within 3 days of an ED evaluation for suspected acute coronary syndrome. Main Outcomes and Measures: The primary outcome was composite risk of death or acute MI, within 30 days of an ED discharge. Results: A total of 79 040 patients were evaluated in this study, of whom 57.7% were female. The mean (SD) age of the cohort was 57 (16) years, and 16 164 patients (21%) had completed early NIT. The absolute risk of death or MI within 30 days was low (<1%). Early NIT had the minor benefit of reducing the absolute composite risk of death or MI (0.4% [95% CI, -0.6% to -0.3%]), and, separately, of death (0.2% [95% CI, -0.2% to -0.1%]), MI (-0.3% [95% CI, -0.5% to -0.1%]), and major adverse cardiac event (-0.5% [95% CI, -0.7% to -0.3%]). The number needed to treat was 250 to avoid 1 death or MI, 500 to avoid 1 death, 333 to avoid 1 MI, and 200 to avoid 1 major adverse cardiovascular event within 30 days. Subgroup analysis revealed a number needed to treat of 14 to avoid 1 death or MI in the subset of patients with elevated troponin. Conclusions and Relevance: Early NIT was associated with a small decrease in the risk of death or MI in patients admitted to the ED with suspected acute coronary syndrome, but this clinical strategy may not be optimal for most patients given the large number needed to treat.

Oligosaccharides composition of Descurainiae sophia exerts anti-heart failure by improving heart function and water-liquid metabolism in rats with heart failure.

PURPOSE: To investigate the protective effect of Oligosaccharides composition of Descurainiae sophia on doxorubicin-induced heart failure in rats, and to study its mechanism. METHOD: A rat model of heart failure was established in 180-220 g male Sprague-Dawley rats by low-dose intraperitoneal injection of doxorubicin for 6 weeks. Four weeks after continuous administration, echocardiography was used to detect left ventricular end diastolic diameter (LVEDD) and end systolic diameter (LVESD) in each group, and left ventricular short axis shortening rate (LVFS) and ejection fraction (LVEF) were calculated. ELISA method was used to detecte the levels of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), troponin I (cTnI), creatine kinase (CK), angiotensin II (Ang II), aldosterone (ALD), arginine pressurization AVP, Renin, Endothelin (ET-1), Nitric Oxide (NO), AQP2 in urine. 6 h cumulative urine output was measured by metabolic cage method after administration for 3 weeks. The urine osmotic pressure was measured by freezing point method. The expression of AQP2 protein in kidney was detected by Western blot method. The changes of myocardial morphology were observed. RESULTS: Compared with the normal control group, the heart rate of the model group was significantly increased (P < 0.01). LVESD and LVEDD were significantly increased (P < 0.01), LVEF and LVFS were significantly decreased (P < 0.01). The levels of CK, cTnI, NO, ET-1, BNP, ANP, ALD, AngII, Renin, AQP2, AVP and osmotic pressure were significantly increased (P < 0.01). Urine output was significantly decreased (P < 0.01). The heart HE showed obvious lesions. Compared with the model group, the Oligosaccharides composition of Descurainiae sophia significantly reduced the heart rate (P < 0.05), decreased LVESD and LVEDD (P < 0.01 or P < 0.05), and increased LVFS and LVEF values (P < 0.01). Oligosaccharides composition of Descurainiae sophia could significantly improve pathological damage of the heart, decrease the levels of cTnI, BNP, AngII, ALD, Renin, AVP in the serum, osmotic pressure and AQP2in the urine (P < 0.01 or P < 0.05), down-regulate the expression of AQP2 protein in the renal(P < 0.01), increase urine volume (P < 0.05). CONCLUSION: Oligosaccharides composition of Descurainiae sophia can significantly improve cardiac function and the disorder of water metabolism in rats with heart failure. Oligosaccharides composition of Descurainiae sophia exerts anti- heart failure through the RAAS system and the arginine vasopressin system.

Management of nonischemic-dilated cardiomyopathies in clinical practice: a position paper of the working group on myocardial and pericardial diseases of Italian Society of Cardiology.

: Nonischemic-dilated cardiomyopathy (NIDCM) is an entity that gathers extremely heterogeneous diseases. This awareness, although leading to continuous improvement in survival, has increased the complexity of NIDCM patients' management. Even though the endorsed 'red-flags' approach helps clinicians in pursuing an accurate etiological definition in clinical practice, it is not clear when and how peripheral centers should interact with referral centers with specific expertise in challenging scenarios (e.g. postmyocarditis and genetically determined dilated cardiomyopathy) and with easier access to second-line diagnostic tools and therapies. This position paper will summarize each step in NIDCM management, highlighting the multiple interactions between peripheral and referral centers, from first-line diagnostic workup and therapy to advanced heart failure management and long-term follow-up.

Spondias mombin L. attenuates ventricular remodelling after myocardial infarction associated with oxidative stress and inflammatory modulation.

The objective of this study was to evaluate Spondias mombin L. (SM) pulp and its influence on cardiac remodelling after myocardial infarction (MI). Male Wistar rats were assigned to four groups: a sham group (animals underwent simulated surgery) that received standard chow (S; n = 20), an infarcted group that received standard chow (MI; n = 24), an infarcted group supplemented with 100 mg of SM/kg bodyweight/d, (MIS100; n = 23) and an infarcted group supplemented with 250 mg of SM/kg bodyweight/d (MIS250; n = 22). After 3 months of treatment, morphological, functional and biochemical analyses were performed. MI induced structural and functional changes in the left ventricle with worsening systolic and diastolic function, and SM supplementation at different doses did not influence these variables as analysed by echocardiography and an isolated heart study (P > .05). However, SM supplementation attenuated cardiac remodelling after MI, reducing fibrosis (P = .047) and hypertrophy (P = .006). Biomarkers of oxidative stress, inflammatory processes and energy metabolism were further investigated in the myocardial tissue. SM supplementation improved the efficiency of energy metabolism and decreased lipid hydroperoxide in the myocardium [group S (n = 8): 267.26 ± 20.7; group MI (n = 8): 330.14 ± 47.3; group MIS100 (n = 8): 313.8 ± 46.2; group MIS250: 294.3 ± 38.0 nmol/mg tissue; P = .032], as well as decreased the activation of the inflammatory pathway after MI. In conclusion, SM supplementation attenuated cardiac remodelling processes after MI. We also found that energy metabolism, oxidative stress and inflammation are associated with this effect. In addition, SM supplementation at the highest dose is more effective.

Cyclovirobuxine D protects against diabetic cardiomyopathy by activating Nrf2-mediated antioxidant responses.

Diabetic cardiomyopathy (DCM) is the principal cause of death in people with diabetes. However, there is currently no effective strategy to prevent the development of DCM. Although cyclovirobuxine D (CVB-D) has been widely used to treat multiple cardiovascular diseases, the possible beneficial effects of CVB-D on DCM remained unknown. The present aim was to explore the potential effects and underlying mechanisms of CVB-D on DCM. We explored the effects of CVB-D in DCM by using high fat high sucrose diet and streptozotocin-induced rat DCM model. Cardiac function and survival in rats with DCM were improved via the amelioration of oxidative damage after CVB-D treatment. Our data also demonstrated that pre-treatment with CVB-D exerted a remarkable cytoprotective effect against high glucose -or H2O2 -induced neonatal rat cardiomyocyte damage via the suppression of reactive oxygen species accumulation and restoration of mitochondrial membrane potential; this effect was associated with promotion of Nrf2 nuclear translocation and its downstream antioxidative stress signals (NQO-1, Prdx1). Overall, the present data has provided the first evidence that CVB-D has potential therapeutic in DCM, mainly by activation of the Nrf2 signalling pathway to suppress oxidative stress. Our findings also have positive implications on the novel promising clinical applications of CVB-D.

[INDICATORS OF CARDIOHEMODYNAMICS OF RHYTHM DISTURBANCES IN ELDERLY PEOPLE WITH CHRONIC HEART FAILURE].

The aim of our study was to study and analyze the electrophysiological indicators of rhythm disturbances in heart failure in elderly people who participated in the elimination of the consequences of the Chernobyl accident in the distant period. In order to assess the functional features, 50 elderly patients (65-74 years old) who participated in the liquidation of the consequences of the Chernobyl accident were examined. Patients were divided into 4 groups depending on the length of stay in an environmentally disadvantaged zone: group 1 (April-June 1986) - 8 (16%) people; 2 (June-December 1986) -14 (28%); 3 (1987-1989) -17 (34%) and group 4 (1990-91gg) -11 (22%) people. All patients were on basic therapy. To study cardiogemodynamics in this category of patients, the following electrophysiological research methods were performed: ECG, XM ECG, SMAD, EchoCG. When analyzing electrophysiological studies, the MSExcel and Statistica programs were used. The examined patients showed a high incidence of left ventricular hypertrophy and cardiac arrhythmias. So in the 1st and 2nd groups, atrial fibrillation, sinus tachy and bradycardia, AV blockade of 1-2 degrees were reliably detected. In groups 3 and 4, left ventricular hypertrophy and arrhythmias were detected with a lower frequency. It should be noted that these changes were observed in individuals participating in the LPA from April to December 1986, i.e. in the first year after the accident. According to echocardiography, diastolic dysfunction of the left ventricle was found mainly in individuals of 1-2 groups. High high indices of KDR, BWW and KSO in 1-2 groups are noted. LVMI exceeds its norm in all studied groups. Thus, statistically significant differences of some indicators are revealed with electrophysiological research methods in all groups of elderly patients with heart failure participating in the liquidation of the Chernobyl accident, as well as the high incidence of rhythm disturbances in patients with Chernobyl nuclear power plants.

Modified citrus pectin ameliorates myocardial fibrosis and inflammation via suppressing galectin-3 and TLR4/MyD88/NF-κB signaling pathway.

Myocardial fibrosis (MF) plays a key role in the development and progression of heart failure (HF) with limited effective therapies. Galectin-3 (Gal-3) is a biomarker associated with fibrosis and inflammation in patients with HF. The Gal-3 inhibitor modified citrus pectin (MCP) protects against cardiac dysfunction, though the underlying mechanism remains unclear. The aim of this study was to investigate the effect and mechanism of MCP on MF using an isoproterenol (ISO)-induced rat model of HF. Cardiac function was analyzed by echocardiography and electrocardiography. Histopathological changes in the heart tissue were assessed by hematoxylin-eosin and Masson trichrome staining. The mRNA and protein expression levels of signaling molecules and pro-inflammatory cytokines were monitored by immunohistochemistry, western blot, qRT-PCR and ELISA analyses. The results demonstrated that MCP ameliorated cardiac dysfunction, decreased myocardial injury and reduced collagen deposition. Furthermore, MCP downregulated the expression of Gal-3, TLR4 and MyD88, thereby inhibiting NF-κB-p65 activation. MCP also decreased the expression of IL-1ß, IL-18 and TNF-α, which have been implicated in the pathogenesis of HF. These inhibitory effects were observed on day 15 and continued until day 22. Taken together, these results suggest that MCP ameliorates cardiac dysfunction through inhibiting inflammation and MF. These effects may be through downregulating Gal-3 expression and suppressing activation of the TLR4/MyD88/NF-κB signaling pathway. The present study supports the use of Gal-3 as a therapeutic target for the treatment of MF after myocardial infarction.

Therapeutic efficacy of shenmai injection as an adjuvant treatment in dilated cardiomyopathy: A protocol for systematic review.

BACKGROUND: Shenmai injection (SMI) is a Traditional Chinese Medicine patent prescription consisting of extractions from ophiopogonis radix and ginseng radix rubra. Clinical studies showed that SMI combined with conventional medicine treatment (CMT) can enhance the therapeutic efficacy for dilated cardiomyopathy (DCM). However, there is still a lack of comprehensive and systematic evidence, which urgently requires us to verify its therapeutic efficacy. Hence, we provide a protocol for systematic review and meta-analysis. METHODS: The systematic search on the MEDLINE/PubMed, China National Knowledge Infrastructure (CNKI), Wanfang database, VIP database, the Cochrane Library, Embase and Chinese Biomedical Database (CBM) in Chinese and English language with dates ranging from the earliest record to August 8, 2019. Next, the quality of each trial was assessed according to the criteria of the Cochrane Handbook for Systematic Reviews of Interventions. Then, the outcome data were recorded and pooled by RevMan 5.3 software. RESULTS: The systematic review and meta-analysis aims to review and pool current clinical outcomes of SMI for the adjuvant treatment of DCM. CONCLUSION: This study will provide a high-quality evidence of SMI for the adjuvant treatment on DCM patients. PROSPERO REGISTRATION NUMBER: CRD42019146369.