scholarly journals Retraction of: Salidroside Protection Against Oxidative Stress Injury Through the Wnt/β-Catenin Signaling Pathway in Rats with Parkinson’s Disease

2021 ◽  
Vol 55 (5) ◽  
pp. 670-670
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Signaling Pathway ◽  
Stress Injury ◽  
Oxidative Stress Injury

Cyclosporin A Protected Cardiomyocytes Against Oxidative Stress Injury by Inhibition of NF-κB Signaling Pathway

2019 ◽  
Vol 10 (2) ◽  
pp. 329-343 ◽  
Author(s):  
Meng Ma ◽  
Xiaohui Ma ◽  
Jie Cui ◽  
Yifeng Guo ◽  
Xiuqin Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclosporin A ◽  
Signaling Pathway ◽  
Stress Injury ◽  
Oxidative Stress Injury

scholarly journals NOX2-Derived Hydrogen Peroxide Impedes the AMPK/Akt-mTOR Signaling Pathway in Parkinson's Disease in Vitro Models

2021 ◽  
Author(s):  
Ruijie Zhang ◽  
Nana Zhang ◽  
Xiaoqing Dong ◽  
Xin Chen ◽  
Jing Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Hydrogen Peroxide ◽  
Parkinson's Disease ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Mtor Signaling ◽  
Regulatory Proteins ◽  
Mtor Signaling Pathway ◽  
Compound C

Abstract Oxidative stress is closely related to the pathogenesis of Parkinson's disease (PD), a typical neurodegenerative disease. NADPH oxidase 2 (NOX2) is involved in hydrogen peroxide (H2O2) generation. Recently, we have reported that H2O2 and PD toxins, including 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenylpyridin-1-ium (MPP+) and rotenone, induce neuronal apoptosis by inhibiting mTOR pathway. Here, we show that 6-OHDA, MPP+ or rotenone induced H2O2 generation by upregulation of NOX2 and its regulatory proteins (p22phox, p40phox, p47phox, p67phox, and Rac1), leading to apoptotic cell death in PC12 cells and primary neurons. Pretreatment with catalase, a H2O2-scavenging enzyme, significantly blocked PD toxins-evoked NOX2-derived H2O2, thereby hindering activation of AMPK, inhibition of Akt/mTOR, induction of apoptosis in neuronal cells. Similar events were also seen in the cells pretreated with Mito-TEMPO, a mitochondria-specific superoxide scavenger, implying a mitochondrial H2O2-dependent mechanism involved. Further research revealed that inhibiting NOX2 with apocynin or silencing NOX2 attenuated the effects of PD toxins on AMPK/Akt/mTOR and apoptosis in the cells. Of importance, ectopic expression of constitutively active Akt or dominant negative AMPKα, or inhibition of AMPK with compound C suppressed PD toxins-induced expression of NOX2 and its regulatory proteins, as well as consequential H2O2 and apoptosis in the cells. Taken together, these results indicate that certain PD toxins can impede the AMPK/Akt-mTOR signaling pathway leading to neuronal apoptosis by eliciting NOX2-derived H2O2. Our findings suggest that neuronal loss in PD may be prevented by regulating of NOX2, AMPK/Akt-mTOR signaling and/or administering antioxidants to ameliorate oxidative stress.

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.

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