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The Regulatory Mechanism and Effect of Receptor-Interacting Protein Kinase 3 on Phenylephrine-Induced Cardiomyocyte Hypertrophy
In this study, we aimed to investigate the regulatory mechanism of RIPK3 on phenylephrine (PE)-induced cardiomyocyte hypertrophy. Cardiomyocyte hypertrophy was induced by exposure to PE (100 μM) for 48 hours. Primary cardiomyocytes were pretreated with RIPK3 inhibitor GSK′872 (10 μM), and RIPK3 siRNA was used to deplete the intracellular expression of RIPK3. The indexes related to myocardial hypertrophy, cell injury, necroptosis, CaMKII activation, gene expression, oxidative stress, and mitochondrial membrane potential were measured. We found that after cardiomyocytes were stimulated by PE, the expressions of hypertrop...
Source: Journal of Cardiovascular Pharmacology - August 1, 2022 Category: Cardiology Tags: Original Article Source Type: research

Upregulation of Periostin Through CREB Participates in Myocardial Infarction-induced Myocardial Fibrosis
This study aims to verify the hypothesis that CREB promotes the expression of periostin in MI-induced myocardial fibrosis. To test this hypothesis, primary rat cardiac fibroblasts were cultured and rat model of MI was established. The level of myocardial fibrosis post-MI was identified by histological staining. The expressions of CREB and periostin were detected through western blot and reverse transcription quantity polymerase chain reaction. The upregulation and downregulation of CREB and periostin were established by plasmid, small interfere RNA (siRNA), and lentivirus, respectively. High levels of CREB and periostin we...
Source: Journal of Cardiovascular Pharmacology - May 1, 2022 Category: Cardiology Tags: Original Article Source Type: research

Xanthoangelol Prevents Ox-LDL–Induced Endothelial Cell Injury by Activating Nrf2/ARE Signaling
Conclusions: These data suggest that XAG cytoprotects against Ox-LDL–induced cell injury through activating Nrf2/ARE–mediated antioxidative stress. Cumulatively, these findings show that EX has the potential to prevent and treat AS.
Source: Journal of Cardiovascular Pharmacology - August 1, 2019 Category: Cardiology Tags: Original Article Source Type: research

Melatonin-Mediated Pak2 Activation Reduces Cardiomyocyte Death Through Suppressing Hypoxia Reoxygenation Injury–Induced Endoplasmic Reticulum Stress
Abstract: Cardiac reperfusion injury has been found to be associated with endoplasmic reticulum (ER) stress. Recently, p21-activated kinase 2 (Pak2) has been identified as a primary mediator of ER stress in chronic myocardial injury. Melatonin, a biological clock–related hormone, has been demonstrated to attenuate heart reperfusion burden by modulating ER stress and mitochondrial function. The aim of our study was to explore whether reperfusion-induced ER stress is modulated by melatonin through Pak2. Hypoxia reoxygenation (HR) was used in vitro to mimic reperfusion injury in cardiomyocytes. ER stress, oxidative stress...
Source: Journal of Cardiovascular Pharmacology - July 1, 2019 Category: Cardiology Tags: Original Article Source Type: research

Mitochondrial Dysfunction and Apoptosis Are Attenuated on κ-Opioid Receptor Activation Through AMPK/GSK-3β Pathway After Myocardial Ischemia and Reperfusion
Abstract: Previous studies have shown that κ-opioid receptor activation possesses cardioprotection against myocardial ischemia and reperfusion (MI/R) injury. The current study was designed to investigate whether mitochondrial dysfunction after MI/R is regulated by the κ-opioid receptor and to further explore the underlying mechanisms involved. MI/R rat model was established in vivo, and a hypoxia and reoxygenation cardiomyocytes model was used in vitro. Mitochondrial morphology and function as well as myocardial apoptosis were determined. Our data indicated that treatment with U50,488H (a selective κ-opioid receptor a...
Source: Journal of Cardiovascular Pharmacology - February 1, 2019 Category: Cardiology Tags: Original Article Source Type: research

Muramyl Dipeptide Induces Reactive Oxygen Species Generation Through the NOD2/COX-2/NOX4 Signaling Pathway in Human Umbilical Vein Endothelial Cells
Abstract: Vascular endothelium dysfunction caused by oxidative stress accelerates the pathologic process of cardiovascular diseases. NOD2, an essential receptor of innate immune system, has been demonstrated to play a critical role in atherosclerosis. Here, the aim of our study was to investigate the effect and underlying molecular mechanism of muramyl dipeptide (MDP) on NOX4-mediated reactive oxygen species (ROS) generation in human umbilical vein endothelial cells (HUVECs). The 2,7-dichlorofluorescein diacetate staining was to measure the intracellular ROS level and showed MDP-promoted ROS production in a time- and dos...
Source: Journal of Cardiovascular Pharmacology - June 1, 2018 Category: Cardiology Tags: Original Article Source Type: research

Rutaecarpine Suppresses Proliferation and Promotes Apoptosis of Human Pulmonary Artery Smooth Muscle Cells in Hypoxia Possibly Through HIF-1α–Dependent Pathways
Conclusions: Our results demonstrated that Rut exerted protective effects on HPASMCs against hypoxia partly through the HIF-1α–dependent signaling pathway.
Source: Journal of Cardiovascular Pharmacology - May 1, 2018 Category: Cardiology Tags: Original Article Source Type: research

Microsomal Prostaglandin E Synthase-1 Expression by Aortic Smooth Muscle Cells Attenuates the Differentiated Phenotype
Abstract: The development of numerous types of cardiovascular disease is associated with alteration of the vascular smooth muscle cell (SMC) phenotype. We have previously shown that abdominal aortic aneurysm progression in a mouse model of the disease is associated with reduced differentiation of SMCs within the lesion and that cyclooxygenase-2 (COX-2) is critical to initiation and progression of the aneurysms. The current studies used human aortic SMC (hASMC) cultures to better characterize mechanisms responsible for COX-2-dependent modulation of the SMC phenotype. Depending on the culture conditions, hASMCs expressed mul...
Source: Journal of Cardiovascular Pharmacology - August 1, 2016 Category: Cardiology Tags: Original Article Source Type: research

CTRP9 Ameliorates Pulmonary Arterial Hypertension Through Attenuating Inflammation and Improving Endothelial Cell Survival and Function
In conclusion, CTRP9 ameliorated PH by attenuating inflammation and improving endothelial cell survival and function.
Source: Journal of Cardiovascular Pharmacology - May 1, 2016 Category: Cardiology Tags: Original Article Source Type: research

microRNA-29b Mediates the Antifibrotic Effect of Tanshinone IIA in Postinfarct Cardiac Remodeling
Conclusions: TSN exerts antifibrotic effects in postinfarct cardiac fibrosis by upregulating the expression of miR-29b, which is mediated by the TGF-β–Smad3 signaling pathway.
Source: Journal of Cardiovascular Pharmacology - May 1, 2015 Category: Cardiology Tags: Original Article Source Type: research

Critical Role of Prohibitin in Endothelial Cell Apoptosis Caused by Glycated Low-density Lipoproteins and Protective Effects of Grape Seed Procyanidin B2
In this study, we showed that glyLDL treatment decreased protein level of PHB, reduced viability, and increased apoptosis in human umbilical vein endothelial cells (HUVEC). PHB overexpression or GSPB2 significantly attenuated apoptosis induced by glyLDL. Moreover, PHB siRNA increased HUVEC apoptosis, along with defective mitochondria and increased levels of cytosol cytochrome c concentration, caspase-3 activity, Bax/Bcl-2 ratio, and phosphorylated Akt, whereas PHB overexpression or GSPB2 restored these changes. Our study identified PHB as an important player responsible for HUVEC apoptosis induced by glyLDL. GSPB2 protecte...
Source: Journal of Cardiovascular Pharmacology - January 1, 2015 Category: Cardiology Tags: Original Article Source Type: research

Cytoprotection of Baicalein Against Oxidative Stress-induced Cardiomyocytes Injury Through the Nrf2/Keap1 Pathway
Abstract:Baicalein is one of the major flavonoids found in the root of Scutellaria baicalensis Georgi. Previous studies suggest that baicalein displays protective effect on experimental cardiac models in vitro and in vivo. However, the mode of action remains unclear. Here, we showed that baicalein conferred cardioprotective effect against oxidative stress-induced cell injury in H9c2 cells and human embryonic stem cells-derived cardiomyocytes. Immunoprecipitation with anti-NF-E2–related factor 2 (Nrf2) antibody in baicalein-treated cells demonstrated that baicalein effectively disrupted the association between Nrf2 and Ke...
Source: Journal of Cardiovascular Pharmacology - January 1, 2015 Category: Cardiology Tags: Original Article Source Type: research

Statin Inhibits the Expression of Secretory Phospholipase A2 and Subsequent Monocyte Chemoattractant Protein-1 in Human Endothelial Cells
We reported that tumor necrosis factor-alpha (TNFα) enhanced the expression of group V PLA2 (sPLA2-V) in human umbilical vein endothelial cells (HUVECs), and the LPC content in LDL and the monocyte chemoattractant protein-1 (MCP-1) expression were augmented when TNFα-stimulated HUVECs were incubated with LDL. Here, we observed that an HMG-CoA reductase inhibitor, pitavastatin, at the concentration of>1 μM administered 12 hours before TNFα stimulation suppressed the enhancement of sPLA2-V mRNA and protein. Pitavastatin also prevented the enhancement of the LPC content in LDL and the expression of MCP-1 mRNA when TNFα-s...
Source: Journal of Cardiovascular Pharmacology - December 1, 2014 Category: Cardiology Tags: Original Article Source Type: research