The Mitochondrial-Derived Peptide MOTS-c Attenuates Oxidative Stress Injury and the Inflammatory Response of H9c2 Cells Through the Nrf2/ARE and NF-κB Pathways

2021 ◽  
Author(s):  
Caijie Shen ◽  
Jian Wang ◽  
Mingjun Feng ◽  
Jianye Peng ◽  
Xiangfeng Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
H9c2 Cells ◽  
Stress Injury ◽  
Oxidative Stress Injury

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.

scholarly journals Rhubarb-Aconite Decoction (RAD) Drug-Containing Serum Alleviated Endotoxin-Induced Oxidative Stress Injury and Inflammatory Response in Caco-2 Cells In Vitro

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xiao-hong Du ◽  
Qing-jun Chen ◽  
Jian-bo Song ◽  
Yan Xie ◽  
Yan Zhi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Calcium Ion ◽  
Lipid Peroxide ◽  
Intestinal Injury ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Stress Injury ◽  
Oxidative Stress Injury

Rhubarb-Aconite Decoction (RAD), a famous Chinese medicine prescription, has been widely used for treating intestinal injury. However, the effect of RAD on intestinal epithelial cells is unclear. The aim of this study was to investigate the effects of RAD drug-containing serum on the oxidative stress injury and inflammatory response induced by endotoxin (ET) in Caco-2 cells in vitro. Lipid peroxide malondialdehyde (MDA), lactate dehydrogenase (LDH), caspase-11, tumor necrosis factor-α(TNF-α), interleukin-3(IL-3), and cytokeratin (CK)18, adenosine triphosphate (ATP) activity, and intracellular free calcium ion levels were measured. The results showed that ET triggered the activation of caspase-11 and the massive release of TNF-α, increased the inhibitory rate of cell growth, MDA, and LDH expressions in Caco-2 cells. Moreover, RAD drug-containing serum could inhibit caspase-11 activation, decrease the release of TNF-α and IL-3, reduce intracellular free calcium ion, and enhance CK 18 expression and ATP activity. These novel findings demonstrated that ET-induced oxidative stress injury and inflammatory response of Caco-2 cells were improved by RAD drug-containing serum, indicating that RAD may be a good choice for the treatment of intestinal injury.

scholarly journals Effect of lentivirus-mediated CFTR overexpression on oxidative stress injury and inflammatory response in the lung tissue of COPD mouse model

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Xiaoli Xu ◽  
Huimin Huang ◽  
Xiangyi Yin ◽  
Hongmei Fang ◽  
Xiaoyue Shen
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Negative Control ◽  
Chronic Obstructive ◽  
Stress Injury ◽  
Obstructive Pulmonary Disease ◽  
Oxidative Stress Injury

Abstract We aimed to investigate the regulatory mechanism of lentivirus-mediated overexpression of cystic fibrosis transmembrane conductance regulator (CFTR) in oxidative stress injury and inflammatory response in the lung tissue of mouse model of chronic obstructive pulmonary disease (COPD). COPD mouse model induced by cigarette smoke was established and normal mice were used as control. The mice were assigned into a normal group (control), a model group (untreated), an oe-CFTR group (injection of lentivirus overexpressing CFTR), and an oe-NC group (negative control, injection of lentivirus expressing irrelevant sequences). Compared with the oe-NC group, the oe-CFTR group had higher CFTR expression and a better recovery of pulmonary function. CFTR overexpression could inhibit the pulmonary endothelial cell apoptosis, reduce the levels of glutathione (GSH), reactive oxygen species (ROS), and malondialdehyde (MDA) and increase the values of superoxide dismutase (SOD), GSH peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). The overexpression also led to reductions in the white blood cell (WBC) count in alveolus pulmonis, the concentrations of C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor-α, and the protein expressions of NF-κB p65, ERK, JNK, p-EPK, and p-JNK related to MAPK/NF-κB p65 signaling pathway. In conclusion, CFTR overexpression can protect lung tissues from injuries caused by oxidative stress and inflammatory response in COPD mouse model. The mechanism behind this may be related to the suppression of MAPK/NF-κB p65 signaling pathway.

scholarly journals Insulin alleviates the inflammatory response and oxidative stress injury in cerebral tissues in septic rats

2014 ◽  
Vol 11 (1) ◽  
pp. 18 ◽  
Author(s):  
Qiyi Chen ◽  
Wenkui Yu ◽  
Jiangliang Shi ◽  
Juanhong Shen ◽  
Tao Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

Biodegradable BiOCl Platform for Oxidative Stress Injury–Enhanced Chemodynamic/Radiation Therapy of Hypoxic Tumors

2021 ◽  
Author(s):  
Yongtian Liu ◽  
Jing Zhang ◽  
Jun Du ◽  
Kang Song ◽  
Jinliang Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Radiation Therapy ◽  
Stress Injury ◽  
Oxidative Stress Injury

Prevention of Oxidative Stress Injury to Sperm

2005 ◽  
Vol 26 (6) ◽  
pp. 654-660 ◽  
Author(s):  
A. Agarwal
Keyword(s):  
Oxidative Stress ◽  
Stress Injury ◽  
Oxidative Stress Injury
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