Boosting mTOR-Dependent Autophagy Via Upstream TLR4-MyD88-MAPK Signaling and Downstream NF-κB Pathway Quenches Intestinal Inflammation and Oxidative Stress Injury

2018 ◽  
Author(s):  
Mingxia Zhou ◽  
Weimin Xu ◽  
Jiazheng Wang ◽  
Junkai Yan ◽  
Yingying Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intestinal Inflammation ◽  
Mapk Signaling ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

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.

scholarly journals Puerarin Attenuates LPS-Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Xing Chang ◽  
Tian Zhang ◽  
Dong Liu ◽  
Qingyan Meng ◽  
Peizheng Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quality Control ◽  
Endothelial Cells ◽  
Protective Effect ◽  
Umbilical Vein ◽  
Mitochondrial Quality Control ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Umbilical Vein Endothelial Cells ◽  
And Oxidative Stress

Atherosclerosis is closely associated with the inflammatory reaction of vascular endothelial cells. Puerarin (Pue), the main active component isolated from the rhizome of Pueraria lobata, is an isoflavone compound with potent antioxidant properties. Although Pue exhibits promising antiatherosclerotic pharmacological effects, only a few studies have reported its protective effect on endothelial cells. This study found that Pue could partly regulate mitochondrial function in human umbilical vein endothelial cells (HUVECs) and reduce or inhibit lipopolysaccharide-induced inflammatory reactions and oxidative stress injury in HUVECs, likely via mitochondrial quality control. Furthermore, the protective effect of Pue on HUVECs was closely related to the SIRT-1 signaling pathway. Pue increased autophagy and mitochondrial antioxidant potential via increased SIRT-1 expression, reducing excessive production of ROS and inhibiting the expression of inflammatory factors and oxidative stress injury. Therefore, Pue may improve mitochondrial respiratory function and energy metabolism, increasing the vulnerability of HUVECs to an inflammatory state.

scholarly journals Ceftriaxone Calcium Crystals Induce Acute Kidney Injury by NLRP3-Mediated Inflammation and Oxidative Stress Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Zhang Yifan ◽  
Ning Benxiang ◽  
Xu Zheng ◽  
Xu Luwei ◽  
Zhou Liuhua ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Injury ◽  
Oxidative Stress Markers ◽  
Stress Injury ◽  
Stress Markers ◽  
Oxidative Stress Injury ◽  
Calcium Crystals ◽  
And Oxidative Stress

Objective. To investigate the role of inflammatory reactions and oxidative stress injury in the mechanisms of ceftriaxone calcium crystal-induced acute kidney injury (AKI) both in vivo and in vitro. Methods. Male Sprague Dawley rats were randomly divided into five groups of ten each according to different concentrations of ceftriaxone and calcium. Based on the levels of serum creatinine (Scr) and blood urea nitrogen (BUN), the AKI group was chosen for the subsequent experiments. Kidney histological examination and immunohistochemistry were performed. The expression of NLRP3 and IL-1β protein and the concentrations of oxidative stress markers such as ROS, MDA, and H2O2 in kidney tissues were estimated. In parallel, HK-2 human renal proximal tubule cells were exposed to ceftriaxone calcium crystals. The mRNA expression levels of NLRP3 and IL-1β and the concentrations of oxidative stress markers were evaluated. Finally, cell viability and rat survival were also assessed. Results. The results showed that significantly increased Scr and BUN levels, consistent with morphological changes and kidney stones, were found in the rats that received the highest concentration of ceftriaxone (1000 mg/kg) combined with calcium (800 mg/kg). The activation of the NLRP3 inflammasome axis and the marked elevation of MDA, H2O2, and ROS levels were observed both in vivo and in vitro. High expression of Nrf2, HO-1, and NQO1 was also documented. In addition, cell apoptosis and rat mortality were promoted by ceftriaxone calcium crystals. Conclusions. Notably, we found that ceftriaxone-induced urolithiasis was associated with a high risk of AKI and NLRP3-mediated inflammasome and oxidative stress injury were of major importance in the pathogenesis.

scholarly journals Chicken bone marrow mesenchymal stem cells improve lung and distal organ injury

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hexuan Niu ◽  
Hanan Song ◽  
Yuhan Guan ◽  
Xianchun Zong ◽  
Ruili Niu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Inflammatory Cytokine ◽  
Organ Injury ◽  
Stress Injury ◽  
Chicken Bone ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

AbstractMesenchymal stem cells (MSCs) are associated with pulmonary protection and longevity. We separated chicken bone marrow-derived mesenchymal stem cells (BM-MSCs); investigated whether BM-MSCs can improve lipopolysaccharide (LPS)-induced lung and distal organ injury; and explored the underlying mechanisms. Ninety-six male ICR (6 weeks old) mice were randomly divided into three groups: Sham, LPS, and LPS + MSC groups. The mice were intratracheally injected with 5 mg/kg LPS to induce acute lung injury (ALI). The histopathological severity of injury to the lung, liver, kidney, heart, and aortic tissues was detected. Wet/dry ratio, protein concentrations in bronchoalveolar lavage fluid (BALF), BALF cell counts, inflammatory cytokine levels in serum, inflammatory cytokine gene expression, and oxidative stress-related indicators were detected. In addition, a survival analysis was performed in sixty male ICR mice (6 weeks old, 18–20 g). This study used chicken BM-MSCs, which are easier to obtain and more convenient than other animal or human MSCs, and have MSC-associated properties, such as a colony forming ability, multilineage differentiation potential, and certain phenotypes. BM-MSCs administration significantly improved the survival rate, systemic inflammation, and the histopathological severity of lung, liver, kidney, and aortic injury during ALI. BM-MSCs administration reduced the levels of inflammatory factors in BALF, the infiltration of neutrophils, and oxidative stress injury in lung tissue. In addition, BM-MSCs administration reduced TRL4 and Mdy88 mRNA expression during ALI. Chicken BM-MSCs serve as a potential alternative resource for stem cell therapy and exert a prominent effect on LPS-induced ALI and extrapulmonary injury, in part through TRL4/Mdy88 signaling and inhibition of neutrophil inflammation and oxidative stress injury.

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