phenanthrenes and Heart-Failure

Sodium tanshinone ⅡA sulfonate (STS) injection has been widely used to treat heart failure over the past years in China. However, to the best of our knowledge, neither systematic review nor meta-analysis on the efficacy of STS injection as adjunctive therapy for heart failure has been reported.. The aim of this study is to summarize relevant evidence from the published randomized controlled trials (RCTs) to evaluate the efficacy of STS injection as adjunctive therapy for heart failure.. RCTs on STS injection as adjunctive therapy for the treatment of heart failure were screened from China National Knowledge Infrastructure (CNKI), Wanfang Database, Sino-Med, PubMed, Google Scholar, Medline, China Science and Technology Journal Database (VIP), Chinese Biomedical Literature Database, Cochrane Library, Embase and Chinese Science Citation Database until July 2021. Two authors independently performed the literature searching, data extraction, and quality evaluation. The meta-analysis was carried out by RevMan 5.3. Based on the methodological quality, years of publication, and sample size of the included RCTs, sensitivity analysis and subgroup analysis were investigated.. Fourteen RCTs with a total of 1368 patients were identified in this study. Results from this meta-analysis showed that STS injection as adjunctive therapy was superior to western medicine alone for the treatment of heart failure in improving the total effective rate (RR = 1.23; 95% CI, 1.17 to 1.29; p < 0.00001) and the left ventricular ejection fraction (LVEF; MD = 6.34; 95% CI 5.25 to 7.43; p < 0.00001), meanwhile reducing the left ventricular end-diastolic diameter (LVEDD; MD = -4.79; 95% CI, -6.44 to -3.15; p < 0.00001), left ventricular end-systolic dimension (LVESD; MD = -3.98; 95% CI, -5.79 to -2.17; p < 0.0001) and brain natriuretic peptide (BNP; MD = -118.75; 95% CI, -175.36 to -62.15; p < 0.0001).. This study indicated that STS injection as adjunctive therapy seemed to be more effective than western medicine alone in treating heart failure. However, due to the poor methodological quality of the included RCTs, further well-designed RCTs are required to confirm the efficacy of STS injection.

Topics: Heart Failure; Humans; Phenanthrenes; Randomized Controlled Trials as Topic; Stroke Volume; Ventricular Function, Left

To study the possible mechanism of ghrelin in heart failure and how it works.. In vitro results demonstrated that ghrelin alleviates cardiac function and reduces myocardial fibrosis in rats with heart failure. Moreover, ghrelin intervention increased PTEN expression level and reduced ERK, c-jun, and c-Fos expression level; in vivo experiments demonstrated that ghrelin intervention reduces mast memory expression and increases cardiomyocyte surface area, PTEN expression level, ERK, c-jun, c-Fos expression level, and cell surface area, while ERK blockade suppresses mast gene expression and reduces cell surface area.. In vitro experimental results prove that we have successfully constructed a rat model related to heart failure, and ghrelin can alleviate the heart function of heart failure rats and reduce myocardial fibrosis. In addition, ghrelin is closely related to the decrease of the expression levels of ERK, c-jun, and c-Fos, but it can also increase the expression of PTEN in the rat model; in vivo experiments proved that we successfully constructed an in vitro cardiac hypertrophy model, and the intervention of ghrelin would reduce the expression of hypertrophic memory and increase the surface area of cardiomyocytes, increase the expression level of PTEN, and reduce the expression levels of ERK, c-jun, and c-Fos, while the blockade of PTEN will increase the expression of hypertrophy genes and increase the cell surface area, while the blockade of ERK will increase the expression of hypertrophic genes, which in turn will make the cell surface area reducing.. Ghrelin inhibits the phosphorylation and nuclear entry of ERK by activating PTEN, thereby controlling the transcription of hypertrophic genes, improving myocardial hypertrophy, and enhancing cardiac function.

Topics: Animals; Butadienes; Cell Enlargement; Cell Line; Computational Biology; Disease Models, Animal; Female; Fibrosis; Gene Expression; Ghrelin; Heart Failure; MAP Kinase Signaling System; Mast Cells; Myocytes, Cardiac; Nitriles; Phenanthrenes; PTEN Phosphohydrolase; Rats; Rats, Sprague-Dawley

Cardiovascular diseases (CVDs) have been associated with environmental pollutants. The scope of this study is to assess any potential relation of polycyclic aromatic hydrocarbons (PAHs), their hydroxylated derivatives, and trace elements with heart failure via their direct determination in human serum of Greek citizens residing in different areas. Therefore, we analyzed 131 samples including cases (heart failure patients) and controls (healthy donors), and the respective demographic data were collected. Significantly higher concentrations (

Topics: Adult; Aged; Aged, 80 and over; Air Pollutants; Air Pollution; Environmental Monitoring; Environmental Pollutants; Female; Fluorenes; Greece; Heart Failure; Humans; Male; Middle Aged; Phenanthrenes; Pilot Projects; Polycyclic Aromatic Hydrocarbons; Principal Component Analysis; Regression Analysis; Sex Factors; Smoking; Surveys and Questionnaires; Trace Elements

Topics: Animals; Apoptosis; Cardiotonic Agents; Cells, Cultured; Disease Models, Animal; DNA Methylation; Epigenesis, Genetic; Heart Failure; Humans; Kelch-Like ECH-Associated Protein 1; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium; NF-E2-Related Factor 2; Oxidative Stress; Phenanthrenes; Promoter Regions, Genetic

Topics: Animals; ATP Binding Cassette Transporter, Subfamily B, Member 1; Digoxin; Dose-Response Relationship, Drug; Down-Regulation; Drug Synergism; Drugs, Chinese Herbal; Female; Fetal Heart; Heart Failure; Lactates; Mice; Mice, Inbred C57BL; Phenanthrenes; Placenta; Pregnancy; Random Allocation; Treatment Outcome

We investigated the effects of a novel ultrapotent poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, PJ34, on cardiac and endothelial dysfunction in a rat model of chronic heart failure (CHF).. Overactivation of the nuclear enzyme PARP importantly contributes to the development of cell dysfunction and tissue injury in various pathophysiologic conditions associated with oxidative stress, including myocardial reperfusion injury, heart transplantation, stroke, shock, and diabetes.. Chronic heart failure was induced in Wistar rats by chronic ligation of the left anterior descending coronary artery. Left ventricular (LV) function and ex vivo vascular contractility and relaxation were measured 10 weeks after the surgery. Nitrotyrosine (NT) formation and PARP activation were detected by immunohistochemistry.. Chronic heart failure induced increased NT formation and PARP activation in the myocardium and intramural vasculature, depressed LV performance, and impaired vascular relaxation of aortic rings. PJ34 significantly decreased myocardial PARP activation but not NT formation, and improved both cardiac dysfunction and vascular relaxation.. Poly(ADP-ribose) polymerase inhibition represents a novel approach for the experimental treatment of CHF.

Topics: Animals; Enzyme Activation; Enzyme Inhibitors; Heart Failure; Immunohistochemistry; Male; Phenanthrenes; Poly(ADP-ribose) Polymerase Inhibitors; Rats; Rats, Wistar; Tyrosine; Vasomotor System; Ventricular Function, Left

Topics: Glycyrrhiza; Heart Failure; Humans; Hyperaldosteronism; Male; Middle Aged; Phenanthrenes; Plants, Medicinal