scholarly journals Ezetimibe Improves Rosuvastatin Effects on Inflammation and Vascular Endothelial Function in Acute Coronary Syndrome Patients Undergoing PCI

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Changqing Sun ◽  
Wuyang Zheng ◽  
Ling Liang ◽  
Zuheng Liu ◽  
Wenchao Sun ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Cell Adhesion ◽  
Endothelial Function ◽  
Cell Adhesion Molecule ◽  
Combination Group ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Coronary Syndrome ◽  
Rosuvastatin Group ◽  
Cell Adhesion Molecule 1

Background. Little is known of the acute effects of ezetimibe in patients with acute coronary syndrome (ACS) undergoing PCI. We investigated whether ezetimibe improves inflammation and vascular endothelial function in patients with ACS undergoing PCI. Methods. We randomized 171 patients with ACS undergoing PCI to receive ezetimibe 10 mg/day plus rosuvastatin 20 mg/day (combination group, n = 81) versus rosuvastatin 20 mg/day (rosuvastatin group, n = 90). Lipid profile, type II secretory phospholipase A2 (sPLA2-IIa), interleukin-1β (IL-1β), vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1) were measured at baseline and after 7 days. Three months after PCI, clinical outcomes were examined. Result. The levels of sPLA2-IIa and IL-1β reduced significantly in both groups, but more when ezetimibe and rosuvastatin were coadministered (sPLA2-IIa: 6.16 ± 2.67 vs. 7.42 ± 3.53 ng/ml, p = 0.01 ; IL-1β: 37.39 ± 26.25 vs. 48.98 ± 32.26 pg/ml, p = 0.01 ). A significant rise of VCAM-1 and ICAM-1 was observed on day 7 after PCI in the both groups, but was less in the combination group (VCAM-1: 918.28 ± 235.31 vs. 988.54 ± 194.41 ng/ml, p = 0.03 ; ICAM-1: 213.01 ± 100.15 vs. 246.88 ± 105.71 ng/ml, p = 0.03 ). Patients in the combination versus rosuvastatin group appeared to suffer from less major adverse events. Periprocedural therapy of ezetimibe improves rosuvastatin effects on proinflammatory responses and endothelial function associated with ACS patients undergoing PCI. This trial is registered with https://clinicaltrials.gov/ct2/show/ChiCTR-IPR-17012219 (Chinese Clinical Trial Registry, http://www.chictr.org.cn on 02/08/2017).

scholarly journals Chronic effects of a high-fat diet enriched with virgin olive oil and a low-fat diet enriched with α-linolenic acid on postprandial endothelial function in healthy men

2008 ◽  
Vol 100 (1) ◽  
pp. 159-165 ◽  
Author(s):  
F. Fuentes ◽  
J. López-Miranda ◽  
P. Pérez-Martínez ◽  
Y. Jiménez ◽  
C. Marín ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Function ◽  
Linolenic Acid ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Low Fat ◽  
Healthy Men ◽  
Low Fat Diet ◽  
Fat Diets ◽  
Cell Adhesion Molecule 1

Traditional cardiovascular risk factors are associated with endothelial dysfunction. The vascular endothelium plays a key role in local vascular tone regulation and can be modulated by dietary fat. We propose to determine the chronic effect of three diets with different fat compositions on postprandial endothelial function and inflammatory biomarkers. Twenty healthy men followed three 4-week diets in a randomised cross-over design: a Western diet, rich in saturated fat (22 % SFA, 12 % MUFA and 0·4 % α-linolenic acid (ALA), all fractions are % of energy); a Mediterranean diet, rich in MUFA ( < 10 % SFA, 24 % MUFA and 0·4 % ALA); a low-fat diet enriched in ALA ( < 10 % SFA, 12 % MUFA and 2 % ALA). At the end of each dietary period all subjects underwent a postprandial study. Plasma concentrations of lipid parameters, soluble intercellular cell-adhesion molecule-1, soluble vascular cell-adhesion molecule-1 (sVCAM-1), nitrates and nitrites (NOx) and endothelial function studied by laser Doppler were examined at 0, 2, 4, 6 and 8 h. The endothelium-dependent vasodilatory response was greater 4 h after the ingestion of the MUFA-rich diet than after the SFA or ALA low-fat diets (P = 0·031). The 4 h postprandial plasma sVCAM-1 levels were lower after the MUFA meals than after the ALA low-fat diet (P = 0·043). The bioavailability of NOx was higher following the MUFA diet than after the SFA and ALA low-fat diets (P = 0·027). We found no differences in the other parameters measured. Chronic ingestion of a Mediterranean diet avoids the postprandial deterioration of endothelial function associated with Westernised diets in healthy individuals.

scholarly journals CircRNA RSF1 regulated ox-LDL induced vascular endothelial cells proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in atherosclerosis

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Xiaohao Zhang ◽  
Junying Lu ◽  
Qinghua Zhang ◽  
Qiang Luo ◽  
Bin Liu
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Luciferase Reporter ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Apoptosis And Inflammation ◽  
Cell Adhesion Molecule 1

Abstract Background Atherosclerosis (AS) is the most common type in cardiovascular disease. Due to its complex pathogenesis, the exact etiology of AS is unclear. circRNA has been shown to play an essential role in most diseases. However, the underlying mechanism of circRNA in AS has been not understood clearly. Methods Quantitative Real-Time PCR assay was used to detect the expression of circRSF1, miR-135b-5p and histone deacetylase 1 (HDAC1). Western blot was applied to the measure of protein expression of HDAC1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), cleaved-caspase-3, vascular cell adhesion molecule 1 (VCAM1), intercellular cell adhesion molecule-1 (ICAM1) and E-selectin. MTT assay and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter assay and RIP assay was used to determine the relationship among circRSF1, miR-135b-5p and HDAC1. Besides, an ELISA assay was performed to measure the levels of IL-1β, IL-6, TNF-α and IL-8. Results In this study, ox-LDL inhibited circRSF1 and HDAC1 expression while upregulated miR-135b-5p expression in Human umbilical vein endothelial cells (HUVECs). Importantly, ox-LDL could inhibit HUVECs growth. Moreover, promotion of circRSF1 or inhibition of miR-135b-5p induced cell proliferation while inhibited apoptosis and inflammation of ox-LDL-treated HUVECs, which was reversed by upregulating miR-135b-5p or downregulating HDCA1 in ox-LDL-treated HUVECs. More than that, we verified that circRSF1 directly targeted miR-135b-5p and HDAC1 was a target mRNA of miR-135b-5p in HUVECs. Conclusion CircRSF1 regulated ox-LDL-induced vascular endothelial cell proliferation, apoptosis and inflammation through modulating miR-135b-5p/HDAC1 axis in AS, providing new perspectives and methods for the treatment and diagnosis of AS.

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