Objective: To investigate the effects of fenofibrate on the proliferation and apoptosis and endothelial nitric oxide synthase (eNOS) mRNA expression of cultured human umbilical vein endothelial cells (HUVECs) induced by lysophosphatidylcholine (LPC).
Methods: HUVECs were cultured in vitro. The study was designated to 5 groups according to fenofibrate concentration: control group, LPC group, LPC + low-concentration fenofibrate (10 micromol/L), LPC + middle-concentration fenofibrate (50 micromol/L), and LPC + high-concentration fenofibrate (100 micromol/L). The study was designated to 6 groups according to the intervention time: control group, LPC group, LPC + fenofibrate (50 micromol/L) 6 h, LPC + fenofibrate 12 h, LPC + fenofibrate 24 h, and LPC + fenofibrate 48 h. The proliferation and apoptosis of HUVECs were evaluated by MTT assay, flow cytometry and fluorescence microscopy, respectively. eNOS mRNA were assayed by real time-PCR.
Results: Compared with the control group, LPC could inhibit the proliferation and induce apoptosis, and downregulate eNOS mRNA expression and decrease NO production of HUVECs. Fenofibrate could increase the proliferation and decrease the apoptosis, and up-regulate eNOS mRNA expression and enhance NO production in HUVECs.
Conclusion: Fenofibrate could improve the proliferation and inhibit the apoptosis, and up-regulate eNOS mRNA expression of HUVECs induced by LPC, which may be responsible for fenofibrate to prevent and treat atherosclerosis.
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Alzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: SARS-CoV-2 causes a variety of neurological sequelae in COVID-19 survivors, including fatigue and cognitive dysfunction. Endothelial dysfunction is the unifying and central mechanism of COVID-19 illness and a major risk factor for vascular dementia (VaD). Endothelial dysfunction stems, in part, from an imbalance between nitric oxide (NO) generated by the endothelial nitric oxide synthase (eNOS) and reactive oxidant species produced by uncoupled-eNOS.
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December 2024
Translational Cardiovascular Medicine UR 3074, FMTS, 1 rue Eugène Boeckel, Strasbourg 67084, France.
Aims: Sodium-glucose co-transporter 2 inhibitors (SGLT2i) show a cardioprotective effect in heart failure and myocardial infarction, pathologies often associated with low-grade inflammation. This cross-sectional study aims to investigate whether low-grade inflammation regulates SGLT2 expression and function in human vasculature, heart, and endothelial cells (ECs).
Methods And Results: Human internal thoracic artery (ITA), left ventricle (LV) specimens, and cultured porcine coronary artery ECs were used.
Mol Biol Rep
December 2024
Department of Basic Medical Sciences, Neyshabur University of Medical Sciences, Neyshabur, Iran.
This study conducts an in-depth review of the correlation between testis tissue changes and circulating microRNAs (miRNA) in diabetes-induced male reproductive complications, drawing upon both animal and clinical studies. The original articles published in English that specifically investigate miRNAs linked to male infertility in humans or animals with either type I or ΙΙ diabetes mellitus were included. The relevant articles were gathered from the PubMed, Google Scholar, Cochrane Library, and ScienceDirect databases.
View Article and Find Full Text PDFCardiovasc Diabetol
December 2024
Department of Cardiology, Xijing Hospital, Air Force Medical University, Xi'an, China.
Background: Adipsin (complement factor D, CFD), as the first described adipokine, is well-known for its regulatory effects in diabetic cardiovascular complications. However, its role in diabetic hind-limb ischemia was not clarified. This study aimed to evaluate the possible therapeutic effect of Adipsin in hind-limb ischemia in type 2 diabetic mice and to elucidate the molecular mechanisms involved.
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