scholarly journals The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

2018 ◽  
Vol 43 (1) ◽  
pp. 191-205 ◽  
Author(s):  
Daoyuan Lv ◽  
Qin Zhou ◽  
Yue Xia ◽  
Xu You ◽  
Zhihong Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Renal Allograft ◽  
Stress Alleviation ◽  
Allograft Dysfunction ◽  
Pathway Activation

scholarly journals Protective Effect of the Aqueous Extract of Deschampsia antarctica (EDAFENCE®) on Skin Cells against Blue Light Emitted from Digital Devices

2020 ◽  
Vol 21 (3) ◽  
pp. 988 ◽  
Author(s):  
Silvia Lorrio ◽  
Azahara Rodríguez-Luna ◽  
Pablo Delgado-Wicke ◽  
Marta Mascaraque ◽  
María Gallego ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Blue Light ◽  
Aqueous Extract ◽  
Electronic Devices ◽  
High Energy ◽  
Dermal Fibroblasts ◽  
Light Irradiation ◽  
Deschampsia Antarctica ◽  
Pathway Activation

Skin is being increasingly exposed to artificial blue light due to the extensive use of electronic devices. This, together with recent observations reporting that blue light—also known as high-energy visible light—can exert cytotoxic effects associated with oxidative stress and promote hyperpigmentation, has sparked interest in blue light and its potential harmful effects on skin. The photoprotective properties of new extracts of different botanicals with antioxidant activity are therefore being studied. Deschampsia antarctica (Edafence®, EDA), a natural aqueous extract, has shown keratinocyte and fibroblast cell protection effects against ultraviolet radiation and dioxin toxicity. In this regard, we studied the protective capacity of EDA against the deleterious effects of artificial blue light irradiation in human dermal fibroblasts (HDF) and melanocytes. We analyzed the impact of EDA on viability, cell morphology, oxidative stress, melanogenic signaling pathway activation and hyperpigmentation in HDF and melanocytes subjected to artificial blue light irradiation. Our results show that EDA protects against cell damage caused by artificial blue light, decreasing oxidative stress, melanogenic signaling pathway activation and hyperpigmentation caused by blue light irradiation. All these findings suggest that EDA might help prevent skin damage produced by artificial blue light exposure from screen of electronic devices.

scholarly journals Autophagy deficiency exacerbates colitis through excessive oxidative stress and MAPK signaling pathway activation

PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225066 ◽  
Author(s):  
Minori Kubota ◽  
Kazuki Kakimoto ◽  
Takatoshi Nakagawa ◽  
Eiko Koubayashi ◽  
Kei Nakazawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Pathway Activation

scholarly journals Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Yunfei Chai ◽  
Zhongming Cao ◽  
Runying Yu ◽  
Yong Liu ◽  
Dongdong Yuan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Signaling Pathway ◽  
Umbilical Vein ◽  
Cx43 Expression ◽  
Ros Signaling ◽  
Pathway Activation ◽  
Carboxyl Terminal ◽  
Umbilical Vein Endothelial Cells ◽  
Inflammation Reaction

Dexmedetomidine is widely used for sedating patients in operation rooms or intensive care units. Its protective functions against oxidative stress, inflammation reaction, and apoptosis have been widely reported. In present study, we explored the effects of dexmedetomidine on monocyte-endothelial adherence. We built lipopolysaccharide- (LPS-) induced monocyte-endothelial adherence models with U937 monocytes and human umbilical vein endothelial cells (HUVECs) and observed the effects of dexmedetomidine on U937-HUVEC adhesion. Specific siRNA was designed to knock-down Connexin43 (Cx43) expression in U937 monocytes. Gö6976, GSK2795039, and NAC were used to inhibit PKC-α, NOX2, and ROS, respectively. Then, we detected whether dexmedetomidine could downregulate Cx43 expression and its downstream PKC-α/NOX2/ROS signaling pathway activation and ultimately result in the decrease of U937-HUVEC adhesion. The results showed that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), could inhibit adhesion of molecule expression (VLA-4 and LFA-1) and U937-HUVEC adhesion. Simultaneously, it also attenuated Cx43 expression in U937 monocytes. With the downregulation of Cx43 expression, the activity of PKC-α and its related NOX2/ROS signaling pathway were reduced. Inhibiting PKC-α/NOX2/ROS signaling pathway with Gö6976, GSK2795039, and NAC, respectively, VLA-4, LFA-1 expression, and U937-HUVEC adhesion were all decreased. In summary, we concluded that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), decreased Cx43 expression in U937 monocytes and PKC-α associated with carboxyl-terminal domain of Cx43 protein. With the downregulation of PKC-α, the NOX2/ROS signaling pathway was inhibited, resulting in the decrease of VLA-4 and LFA-1 expression. Ultimately, U937-HUVEC adhesion was reduced.

scholarly journals Dibromoacetic Acid Induced Hepatotoxicity in Mice through Oxidative Stress and Toll-Like Receptor 4 Signaling Pathway Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Tingting Gong ◽  
Wenbo Jiang ◽  
Zhijian Gao ◽  
Yingying Chen ◽  
Shuying Gao
Keyword(s):  
Oxidative Stress ◽  
Tumor Necrosis Factor ◽  
Signaling Pathway ◽  
Tumor Necrosis ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Dibromoacetic Acid ◽  
Pathway Activation ◽  
Necrosis Factor

Dibromoacetic acid (DBA) is one of haloacetic acids, often as a by-product of disinfection in drinking water. DBA is a multiple-organ carcinogen in rodent animals, but little research on its hepatotoxicity has been conducted and its mechanism has not been elucidated. In this study, we found that DBA could induce obvious hepatotoxcity in Balb/c mice as indicated by histological changes, increasing serum level of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and accumulation of hepatic glycogen, after the mice were administered DBA at doses of 1.25, 5, and 20 mg/kg body weight for 28 days via oral gavage. In mechanism study, DBA induced oxidative stress as evidenced by increasing the level of malondialdehyde (MDA), reactive oxygen species (ROS) in the liver, advanced oxidative protein products (AOPPs) in the serum, and decreasing the level of glutathione (GSH) in the liver. DBA induced inflammation in the liver of the mice which is supported by increasing the production of tumor necrosis factor-α (TNF-α) and the mRNA levels of TNF-α, interleukin-6 (IL-6), interleukin-1β (IL-1β), and nuclear factor κB (NF-κB) in the liver. DBA also upregulated the protein levels of Toll-like receptor (TLR) 4, myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor-associated factor 6 (TRAF6), inhibitor of nuclear factor κB alpha (IκB-α), nuclear factor κB p65 (NF-κB p65), and the phosphoralation of P38 mitogen-activated protein kinase (P38MAPK) and c-Jun N-terminal kinase (JNK). Conclusion. DBA could induce hepatotoxicity in mice by oral exposure; the mechanism is related to oxidative stress, inflammation, and Toll-like receptor 4 signaling pathway activation.

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