Quercetin Alleviates LPS-Stimulated Myocardial Injury through Regulating ALOX5/PI3K/AKT Pathway in Sepsis.

Quercetin (QUE) has been found to inhibit the progression of sepsis-related diseases, including sepsis-induced cardiomyopathy (SIC). More information about the role and mechanism of QUE in SIC progression deserves further exploration. Human cardiomyocytes (AC16) were induced with LPS to mimic SIC cell models.

Chinese herbal medicine therapy for coronary heart disease complicated with anxiety: a systematic review of randomized controlled trials.

Objective: To evaluated the effectiveness and safety of Chinese herbal medicines (CHMs) for coronary heart disease (CHD) complicated with anxiety.

Methods: Randomized controlled clinical trials (RCTs) with parallel-groups were included after searching through electric-databases from inception to May, 2017. Meta-analysis was undertaken with RevMan 5.

Anti-depressive effect of Shuangxinfang on rats with acute myocardial infarction: Promoting bone marrow mesenchymal stem cells mobilization and alleviating inflammatory response.

Bone marrow mesenchymal stem cells (BM-MSCs) are recruited to injured site for cardiac self-repairing in acute myocardial infarction (AMI), but the spontaneous mobilization of BM-MSCs is insufficient for self-repairing. Inflammation initiated by necrosis cardiomyocytes induced cardiac remodeling and depression. Given the anti-inflammatory effects of BM-MSCs and the inextricably relationship among inflammation, ventricular remodeling and depression following AMI, methods focused on enhancing BM-MSCs mobilization are promising.

Chaihulonggumulitang Shows Psycho-cardiology Therapeutic Effects on Acute Myocardial Infarction by Enhancing Bone Marrow Mesenchymal Stem Cells Mobilization.

Ischemic myocardium initiates the mobilization and homing of bone marrow mesenchymal stem cells (BM-MSCs) to promote myocardial regeneration after acute myocardial infarction (AMI). Inflammation caused by necrotic cardiomyocytes induce major pathological changes (cardiac remodeling and myocardial apoptosis) as well as anxiety disorder. This process may be inhibited by the differentiation and paracrine effects of BM-MSCs.