microRNA-218 Inhibits Lipopolysaccharide-Induced Bronchial Epithelial Cell Injury by Targeting E2F2

2020 ◽  
Vol 10 (8) ◽  
pp. 1161-1169
Author(s):  
Min Gong ◽  
Zhongmei Mao ◽  
Jinni Chen ◽  
Xin Ye ◽  
Xiaobing Zhou
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Stress Injury ◽  
Bronchial Epithelial ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

Acute bronchopneumonia is a common hospitalization disease in children and serious acute bronchopneumonia will lead to death of children. MicroRNAs (miRNAs) have been thought to be related to inflammation in many diseases. The present study aimed to investigate the relation between miR218 and E2F2 and the effect of miR-218 overexpression and E2F2 inhibition on the improvement of inflammation in LPS-induced bronchial epithelial cell. BEAS-2B cells were induced by LPS for 0, 6, 12, 24 and 48 h which the cell viability was analyzed by CCK-8 assay. The expression of miR-218 in LPS-induced bronchial epithelial cell and cell transfection was detected by RT-qPCR analysis. The levels of TNF-α, IL-1α, and IL-6 in BEAS2B cells were detected using commercially-available ELISA kits. The levels of ROS, MDA, SOD and LDH were detected by ROS assay kit and oxidative stress assay kit. The cell apoptosis was analyzed by flow cytometry analysis and DAPI and hochest staining. As a result, miR-218 was decreased in LPS-induced bronchial epithelial cell. With the time of LPS treatment extends, the cell viability was decreased. Overexpression of miR-218 reduced the expression of inflammatory cytokines and oxidative stress injury in LPS-induced BEAS2B cells. Overexpression of miR-218 reduced apoptosis of LPS-induced BEAS2B cells. E2F2 was demonstrated be a target of miR-218 which miR-218 overexpression could inhibit the expression of E2F2. E2F2 inhibition could reverse the inflammatory and oxidative stress injury of LPS-induced BEAS2B cells caused by miR-218 inhibition. E2F2 inhibition could reverse the apoptosis of LPS-induced BEAS2B cells caused by miR-218 inhibition. In addition, E2F2 inhibition could reverse the expression of p-STAT1, cleaved-caspase3 and cleaved-caspase9 in LPS-induced BEAS2B cells caused by miR-218 inhibition. In conclusion, this study indicated that miR-218 overexpression and E2F2 inhibition can alleviate the inflammation in LPS-induced bronchial epithelial cell, thereby decreasing the oxidative stress and cell apoptosis.

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

Effects of Atorvastatin Combined with Nano-Selenium on Blood Lipids and Oxidative Stress in Atherosclerotic Rats

2021 ◽  
Vol 21 (2) ◽  
pp. 1331-1337
Author(s):  
Zhe Han ◽  
Yang Wang ◽  
Jing Li
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Endothelial Cell ◽  
High Efficiency ◽  
Biological Effects ◽  
Lipid Lowering ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Combined Use ◽  
And Oxidative Stress

Dyslipidemia and oxidative stress injury of blood vessel walls play important roles in the formation of atherosclerosis (AS) and plaque progression. This is also the main pathological basis for atherosclerosis. Statins, as inhibitors of HMG-CoA reductase in the process of cholesterol biosynthesis, have become key drugs for lipid-lowering treatment. Many studies have found the anti-atherosclerotic effect of atorvastatin is far beyond the lipid-lowering effect. Its lipid-lowering effects are also involved, such as anti-inflammatory, inhibiting endothelial cell ROS production, and improving endothelial cell damage. Nano selenium (Nano-Se) shows stronger anti-oxidation ability, lower toxicity, high efficiency absorption and strong immune regulation ability. Because of the unique biological effects of Nano-Se, it has broad prospects in the field of human health care. Therefore, in this study, by constructing a rat model of abnormal lipid metabolism, we observed changes in parameters such as serum peroxidase (MPO), propylene glycol (MDA), superoxide dismutase (SOD), and blood lipid levels in atherosclerotic rats Happening, furthermore, the effects of atorvastatin+nano-selenium on lipid metabolism disorders and the protective effects and mechanisms of oxidative stress injury in rats were investigated and with a view to providing new targets for the treatment of arteriosclerosis. The results of this study demonstrated that contrast to the AS rat, the combined use of atorvastatin+nano-selenium group could significantly reduce serum TC, TG, and LDL-C contents, and declined tissue lesions such as aortic arch and liver; Significantly enhanced the activities of GPx-1 and SOD in serum, decreased MDA content, and increased the SOD activity in rat aorta. These results suggested that the combined use of atorvastatin+nano-selenium has good protection against oxidative stress caused by disorders of lipid metabolism.

Sign in / Sign up

Export Citation Format

Share Document