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Possibility of Using NO Modulators for Pharmacocorrection of Endothelial Dysfunction After Prenatal Hypoxia.
Pharmaceuticals (Basel)
January 2025
Department of Microbiology, Virology and Immunology, I. Horbachevsky Ternopil State Medical University, 46001 Ternopil, Ukraine.
Prenatal hypoxia (PH) is a key factor in the development of long-term cardiovascular disorders, which are caused by various mechanisms of endothelial dysfunction (ED), including those associated with NO deficiency. This emphasizes the potential of therapeutic agents with NO modulator properties, such as Thiotriazoline, Angiolin, Mildronate, and L-arginine, in the treatment of PH. Pregnant female rats were given a daily intraperitoneal dose of 50 mg/kg of sodium nitrite starting on the 16th day of pregnancy.
View Article and Find Full Text PDFAcute Severe Hypoxia Decreases Mitochondrial Chain Complex II Respiration in Human Peripheral Blood Mononuclear Cells.
Int J Mol Sci
January 2025
Biomedicine Research Center of Strasbourg (CRBS), UR 3072, "Mitochondria, Oxidative Stress and Muscle Plasticity", Faculty of Medicine, University of Strasbourg, 67000 Strasbourg, France.
Peripheral blood mononuclear cells' (PBMCs) mitochondrial respiration is impaired and likely involved in myocardial injury and heart failure pathophysiology, but its response to acute and severe hypoxia, often associated with such diseases, is largely unknown in humans. We therefore determined the effects of acute hypoxia on PBMC mitochondrial respiration and ROS production in healthy volunteers exposed to controlled oxygen reduction, achieving an inspired oxygen fraction of 10.5%.
View Article and Find Full Text PDFRestoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia-Reperfusion Injury Model.
Antioxidants (Basel)
January 2025
Department of Medicinal & Life Science, College of Science and Convergence Technology, Hanyang University-ERICA, Ansan 15588, Republic of Korea.
Cardiac ischemia-reperfusion injury (IRI) occurs when blood flow is restored to the myocardium after a period of ischemia, leading to oxidative stress and subsequent myocardial cell damage, primarily due to the accumulation of reactive oxygen species (ROS). In our previous research, we identified that miR-25 is significantly overexpressed in pressure overload-induced heart failure, and its inhibition improves cardiac function by restoring the expression of SERCA2a, a key protein involved in calcium regulation. In this study, we aimed to investigate the role of miR-25 in the context of ischemia-reperfusion injury.
View Article and Find Full Text PDFeIF4A1 exacerbates myocardial ischemia-reperfusion injury in mice by promoting nuclear translocation of transgelin/p53.
Acta Pharmacol Sin
January 2025
Department of Pharmacology, National Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Medicine Research, Ministry of Education, College of Pharmacy, Harbin Medical University, Harbin, 150086, China.
Eukaryotic translation initiation factor 4A1 (eIF4A1) is an ATP-dependent RNA helicase that participates in a variety of biological and pathological processes such as cell proliferation and apoptosis, and cancer. In this study we investigated the role of eIF4A1 in ischemic heart disease. The myocardial ischemia/reperfusion (I/R) model was established in mice by ligation of the left anterior descending artery for 45 min with the subsequent reperfusion for 24 h; cultured neonatal mouse ventricular cardiomyocytes (NMVCs) treated with HO (200 μM) or H/R (12 h hypoxia and 12 h reoxygenation) were used for in vitro study.
View Article and Find Full Text PDFAbietic Acid Alleviates the Hypoxic Injury of Cardiomyocytes by Adjusting Autophagy and Apoptosis Mediated by miR-30a-5p/GRP78 Axis.
Ann Clin Lab Sci
November 2024
Department of Internal Medicine-Cardiovascular, Hangzhou Xixi Hospital, Hangzhou Sixth People's Hospital, Hangzhou Xixi Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
Objective: To explore the influence of abietic acid on the autophagy and apoptosis of cardiomyocytes in rats with acute myocardial infarction (AMI).
Methods: A rat model of AMI was built by ligation of the anterior descending branch of left coronary artery, and a model of hypoxic cardiomyocyte injury was constructed by treating cardiomyocytes with hypoxia. Western blot assay was used to detect the abundance of proteins related to autophagy and apoptosis, MTT assay was used to measure the viability of cardiomyocytes, and the expression level of miR-30a-5p was detected by qRT-PCR.
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