scholarly journals Recombinant Milk Fat Globule–EGF Factor-8 Reduces Oxidative Stress via Integrin β3/Nuclear Factor Erythroid 2–Related Factor 2/Heme Oxygenase Pathway in Subarachnoid Hemorrhage Rats

Stroke ◽  
2014 ◽  
Vol 45 (12) ◽  
pp. 3691-3697 ◽  
Author(s):  
Fei Liu ◽  
Qin Hu ◽  
Bo Li ◽  
Anatol Manaenko ◽  
Yujie Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Heme Oxygenase ◽  
Milk Fat ◽  
Related Factor ◽  
Nuclear Factor ◽  
Integrin Β3 ◽  
Milk Fat Globule ◽  
Fat Globule

scholarly journals Milk Fat Globule-Epidermal Growth Factor-Factor 8 Reverses Lipopolysaccharide-Induced Microglial Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Jie Li ◽  
Xiaotian Xu ◽  
Xiaoying Cai ◽  
Yinlun Weng ◽  
Yiping Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Milk Fat ◽  
Regulatory Protein ◽  
Milk Fat Globule ◽  
Epidermal Growth ◽  
Fat Globule

Oxidative stress plays an important role in various neurological disorders. Milk fat globule-epidermal growth factor-factor 8 (MFG-E8) is a regulatory protein for microglia. However, its involvement in microglial oxidative stress has not been established. In this study, we observed microglial oxidative stress in response to lipopolysaccharide (LPS) both in vitro and in vivo. LPS induced significant elevation of TNF-α, IL-6, MDA, and ROS and reduction of GSH and SOD in the mouse brains and primary microglia, which were reversed by MFG-E8 pretreatment. MFG-E8 induced the expression of Nrf-2 and HO-1 that was reduced by LPS incubation. Moreover, LPS-increased Keap-1 expression was reversed by MFG-E8. But the above tendencies were not seen when MFG-E8 was applied alone. The current study established the involvement of MFG-E8 in antioxidant effects during neuroinflammation. It may achieve the effects through the regulation of Keap-1/Nrf-2/HO-1 pathways.

scholarly journals Mitophagy Reduces Oxidative Stress Via Keap1 (Kelch-Like Epichlorohydrin-Associated Protein 1)/Nrf2 (Nuclear Factor-E2-Related Factor 2)/PHB2 (Prohibitin 2) Pathway After Subarachnoid Hemorrhage in Rats

Stroke ◽  
2019 ◽  
Vol 50 (4) ◽  
pp. 978-988 ◽  
Author(s):  
Tongyu Zhang ◽  
Pei Wu ◽  
Enkhjargal Budbazar ◽  
Qiquan Zhu ◽  
Chengmei Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Death ◽  
Small Interfering Rna ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Related Factor ◽  
Nuclear Factor ◽  
Interfering Rna

Background and Purpose— Mitoquinone has been reported as a mitochondria-targeting antioxidant to promote mitophagy in various chronic diseases. Here, our aim was to study the role of mitoquinone in mitophagy activation and oxidative stress–induced neuronal death reduction after subarachnoid hemorrhage (SAH) in rats. Methods— Endovascular perforation was used for SAH model of male Sprague-Dawley rats. Exogenous mitoquinone was injected intraperitoneally 1 hour after SAH. ML385, an inhibitor of Nrf2 (nuclear factor-E2-related factor 2), was given intracerebroventricularly 24 hours before SAH. Small interfering RNA for PHB2 (prohibitin 2) was injected intracerebroventricularly 48 hours before SAH. Nuclear, mitochondrial, and cytoplasmic fractions were gathered using nucleus and mitochondria isolation kits. SAH grade evaluation, short- and long- term neurological function tests, oxidative stress, and apoptosis measurements were performed. Pathway related proteins were investigated with Western blot and immunofluorescence staining. Results— Expression of Keap1 (Kelch-like epichlorohydrin-associated protein 1, 2.84× at 24 hours), Nrf2 (2.78× at 3 hours), and LC3II (light chain 3-II; 1.94× at 24 hours) increased, whereas PHB2 (0.46× at 24 hours) decreased after SAH compared with sham group. Mitoquinone treatment attenuated oxidative stress and neuronal death, both short-term and long-term. Administration of mitoquinone resulted in a decrease in expression of Keap1 (0.33×), Romo1 (reactive oxygen species modulator 1; 0.24×), Bax (B-cell lymphoma-2 associated X protein; 0.31×), Cleaved Caspase-3 (0.29×) and an increase in Nrf2 (2.13×), Bcl-xl (B-cell lymphoma-extra large; 1.67×), PINK1 (phosphatase and tensin-induced kinase 1; 1.67×), Parkin (1.49×), PHB2 (1.60×), and LC3II (1.67×) proteins compared with SAH+vehicle group. ML385 abolished the treatment effects of mitoquinone on behavior and protein levels. PHB2 small interfering RNA reversed the outcomes of mitoquinone administration through reduction in protein expressions downstream of PHB2. Conclusions— Mitoquinone inhibited oxidative stress–related neuronal death by activating mitophagy via Keap1/Nrf2/PHB2 pathway after SAH. Mitoquinone may serve as a potential treatment to relieve brain injury after SAH.

scholarly journals Protective Effect of Glutathione against Oxidative Stress-induced Cytotoxicity in RAW 264.7 Macrophages through Activating the Nuclear Factor Erythroid 2-Related Factor-2/Heme Oxygenase-1 Pathway

Antioxidants ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 82 ◽  
Author(s):  
Da Kwon ◽  
Hee-Jae Cha ◽  
Hyesook Lee ◽  
Su-Hyun Hong ◽  
Cheol Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Protective Effect ◽  
Heme Oxygenase ◽  
Raw 264.7 Cells ◽  
Heme Oxygenase 1 ◽  
Raw 264.7 ◽  
Related Factor ◽  
Nuclear Factor ◽  
Raw 264.7 Macrophages

Reactive oxygen species (ROS), products of oxidative stress, contribute to the initiation and progression of the pathogenesis of various diseases. Glutathione is a major antioxidant that can help prevent the process through the removal of ROS. The aim of this study was to evaluate the protective effect of glutathione on ROS-mediated DNA damage and apoptosis caused by hydrogen peroxide, H2O2, in RAW 264.7 macrophages and to investigate the role of the nuclear factor erythroid 2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. The results showed that the decrease in the survival rate of RAW 264.7 cells treated with H2O2 was due to the induction of DNA damage and apoptosis accompanied by the increased production of ROS. However, H2O2-induced cytotoxicity and ROS generation were significantly reversed by glutathione. In addition, the H2O2-induced loss of mitochondrial membrane potential was related to a decrease in adenosine triphosphate (ATP) levels, and these changes were also significantly attenuated in the presence of glutathione. These protective actions were accompanied by a increase in the expression rate of B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein (Bax) and poly(ADP-ribose) polymerase cleavage by the inactivation of caspase-3. Moreover, glutathione-mediated cytoprotective properties were associated with an increased activation of Nrf2 and expression of HO-1; however, the inhibition of the HO-1 function using an HO-1 specific inhibitor, zinc protoporphyrin IX, significantly weakened the cytoprotective effects of glutathione. Collectively, the results demonstrate that the exogenous administration of glutathione is able to protect RAW 264.7 cells against oxidative stress-induced mitochondria-mediated apoptosis along with the activity of the Nrf2/HO-1 signaling pathway.

TMT-Based L6 Quantitative Proteomics Analysis Reveals the Effect of Bovine Derived MFG-E8 against Oxidative Stress on Rat L6 Cells

2021 ◽  
Author(s):  
Guan Kaifang ◽  
He Li ◽  
Haoran Chen ◽  
Xiaofen Qi ◽  
Rongchun Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Milk Fat ◽  
Quantitative Proteomics ◽  
Muscle Injury ◽  
Tissue Homeostasis ◽  
Proteomics Analysis ◽  
L6 Cells ◽  
Milk Fat Globule ◽  
Fat Globule

Milk fat globule-EGF factor 8 (MFG-E8) is a secreted matrix glycoprotein exert a crucial role in regulating tissue homeostasis and protecting against skeletal muscle injury. To explore the molecular mechanism...

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