No abstract

The present study was aimed at investigating the detailed functions of atorvastatin, a lipid-lowering agent, in the pathogenesis of coronary slow flow (CSF), a clinical disease characterized by delayed angiographic coronary opacity without obstructive coronary disease. In the present study, we successfully identified isolated endothelial progenitor cells (EPCs) from the peripheral blood of patients with CSF. Their VEGFA protein levels were determined using immunoblotting analyses. We determined cell viability using MTT assays, cell migration capacity using Transwell assays, and the angiogenic capacity using a tube formation assay. The target association between miR-221 and VEGFA was validated with a luciferase reporter assay. Atorvastatin treatment increased EPC VEGFA protein levels, proliferation, migration, and angiogenesis. miR-221 expression was downregulated after atorvastatin treatment; miR-221 overexpression exerted an opposing effect to atorvastatin treatment on VEGFA protein, EPC proliferation, migration, and angiogenesis. The protective effects of atorvastatin treatment on VEGFA protein and EPCs could be significantly suppressed by miR-221 overexpression. miR-221 directly bound the VEGFA 3'UTR to inhibit its expression. In conclusion, atorvastatin improves the cell proliferation, migration, and angiogenesis of EPCs via the miR-221/VEGFA axis. Thus, atorvastatin could be a potent agent against CSF, pending further in vivo and clinical investigations.

No abstract

Sepsis is a systemic disease caused by bacterial or viral infections. SARS-COV-2, which is still rampant around the world at the end of 2019, can also cause severe viral sepsis. 1,2 Acute lung injury (ALI) is one of the most common complications of sepsis, which can lead to acute respiratory distress syndrome (ARDS) with high mortality. 3 Acute lung injury in sepsis is related to increased pulmonary vascular permeability, alveolar epithelial cell damage, and lung immune inflammatory cell activation and infiltration caused by a large number of inflammatory factors and other substances released during sepsis. 4 However, at present, the pathogenesis of acute lung injury in sepsis has not been fully studied and there is no specific drug treatment.Inflammation disorder is closely related to the pathogenesis of acute lung injury, 5 mainly related to the large release of pro-inflammatory factors and the imbalance of inflammatory factors. 6 Toll-like receptor 4 (TLR4) can specifically recognise