scholarly journals Oviductus Ranae Improves Cognitive Disorder and Suppresses Oxidative Stress in Aging Mice by Activating Nrf2 Pathway

2021 ◽  
Author(s):  
Yuechen Li
Keyword(s):  
Oxidative Stress ◽  
Cognitive Disorder ◽  
Nrf2 Pathway ◽  
Oviductus Ranae

scholarly journals Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Liu Tongqiang ◽  
Liu Shaopeng ◽  
Yu Xiaofang ◽  
Song Nana ◽  
Xu Xialian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Contrast Media ◽  
Renal Injury ◽  
Salvianolic Acid B ◽  
Pi3k Inhibitor ◽  
Iodinated Contrast Media ◽  
Acute Renal Injury ◽  
Nrf2 Pathway ◽  
Salvianolic Acid ◽  
Iodinated Contrast

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.

Propofol alleviates liver oxidative stress via activating Nrf2 pathway

2015 ◽  
Vol 196 (2) ◽  
pp. 373-381 ◽  
Author(s):  
Mian Ge ◽  
Weifeng Yao ◽  
Yanling Wang ◽  
Dongdong Yuan ◽  
Xinjin Chi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nrf2 Pathway

scholarly journals Ox-LDL induced endothelial progenitor cells oxidative stress via p38/Keap1/Nrf2 pathway

2021 ◽  
Author(s):  
Qijun Jiang ◽  
Chengpeng Li ◽  
Zhigang Gong ◽  
Zhigang Li ◽  
Shifang Ding
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Nuclear Translocation ◽  
Tube Formation ◽  
Ros Generation ◽  
Endothelial Progenitor ◽  
Migration Ability ◽  
Nrf2 Pathway

Abstract Background In many studies, endothelial progenitor cells (EPCs) highly expressing antioxidant protein were induced oxidative stress and apoptosis by Oxidized-low density lipoprotein (ox-LDL). Nrf2 which was resently reported to regulate the antioxidant genes and cellular redox regulators was highly expressed in EPCs. However, its role in ox-LDL induced EPCs oxidative stress and apoptosis has not been fully illustrated. Methods EPCs isolated from human peripheral blood mononuclear cells were treated with different concentration of ox-LDL, Keap1 siRNA and a specific p38 MAPK inhibitor SB203580, then used to assay the whole cellular Nrf2 (total Nrf2, t-Nrf2), cytoplasmic Nrf2 (c-Nrf2), nuclear Nrf2 (n- Nrf2), NAD(P) H:quinone oxidoreductase 1 (NQO1) protein levels and Bax /Bcl-2 with western blot, NQO1 mRNA levels with RT-PCR, ROS level with H2DCF-DA, the loss/disruption of mitochondrial membrane potential (MMP) with JC-1, apoptosis with Annexin-V and PI,migration ability with transwell chambers and tube formation. Results The ox-LDL treatment decreased the n-Nrf2/Histone H3 to c-Nrf2/GAPDH ratio, NQO1 mRNA and protein expression levels. Treatment of ox-LDL enhanced the ROS production, induced loss of membrane potential, increase in cell shrinkage, pyknotic nuclei and apoptosis of EPCs. The Keap1 knockdown with Keap1 siRNA increased the nuclear translocation of Nrf2, the NQO1 mRNA and protein transcription levels, and prevented ox-LDL induced ROS generation and formation of JC-1 monomers. Treatment of ox-LDL increased the activation of p38. Pretreatment with SB203580 significantly eliminated ox-LDL induced the inhibition of Nrf2 nuclear translocation, the depression of the mRNA transcription levels of NQO-1, the ROS generation and the formation of JC-1 monomers in EPCs. The pretreatment of Keap1 siRNA decreased the Bax/Bcl-2 ratio which was increased by the treatment of ox-LDL in EPCs. The ox-LDL treatment decreased EPCs migration activity and tube formation. Whereas the pre-treatment with Keap1 siRNA preserved the migration ability and tube formation of EPCs Conclusion Ox-LDL induced EPCs oxidative stress and apoptosis via p38/Keap1/Nrf2 pathway.

scholarly journals NBR1-mediated p62-liquid droplets enhance the Keap1-Nrf2 system

2019 ◽  
Author(s):  
Pablo Sánchez-Martín ◽  
Yu-shin Sou ◽  
Shun Kageyama ◽  
Masaaki Komatsu
Keyword(s):  
Oxidative Stress ◽  
Liquid Droplet ◽  
Brca1 Gene ◽  
Droplet Formation ◽  
Receptor Protein ◽  
Liquid Droplets ◽  
Nrf2 Pathway ◽  
Selective Degradation ◽  
System A ◽  
Nrf2 Activation

Abstractp62/SQSTM1 is a multivalent protein that has an ability to cause a liquid-liquid phase separation and serves as a receptor protein that participates in cargo isolation during selective autophagy. This protein is also involved in the non-canonical activation of the Keap1-Nrf2 system, a major oxidative stress response pathway. Here we show a role of Neighbor of BRCA1 gene 1 (NBR1), an autophagy receptor structurally similar to p62/SQSTM1, in the p62-liquid droplet formation and the Keap1-Nrf2 pathway. The overexpression of NBR1 blocked selective degradation of p62/SQSTM1 through autophagy and promoted the accumulation and phosphorylation of p62/SQSTM1 in liquid-like bodies, which is required for the activation of Nrf2. NBR1 was induced in response to oxidative stress, and then the p62-mediated Nrf2 activation was up-regulated. Conversely, loss of Nbr1 suppresses not only the formation of p62/SQSTM1-liquid droplets but also p62-dependent Nrf2 activation during oxidative stress. Taken together, our results show that NBR1 mediates p62/SQSTM1-liquid droplet formation to activate the Keap1-Nrf2 pathway.

scholarly journals Quantification and cytoprotection by vanillin, 4-methylguaiacol and 4-ethylguaiacol against AAPH-induced abnormal oxidative stress in HepG2 cells

RSC Advances ◽  
2018 ◽  
Vol 8 (62) ◽  
pp. 35474-35484 ◽  
Author(s):  
Dongrui Zhao ◽  
Dongmei Shi ◽  
Jinyuan Sun ◽  
Hehe Li ◽  
Mouming Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Nrf2 Pathway

Vanillin, 4-methylguaiacol, and 4-ethylguaiacol widely exist in Gujinggong Chinese baijiu and could protect HepG2 cells against oxidative stress via activating the Nrf2 pathway.

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