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The inhibition of GSK-3β promotes the production of reactive oxygen species via β-catenin/C/EBPα signaling in the spleen of zebrafish (Danio rerio).
- Source :
-
Fish & Shellfish Immunology . May2018, Vol. 76, p110-120. 11p. - Publication Year :
- 2018
-
Abstract
- In this study, the mechanism that the inhibition of glycogen synthase kinase-3β (GSK-3β) promotes the production of reactive oxygen species (ROS) via β-catenin/CCAAT/enhancer binding protein α (C/EBPα) signaling was investigated in the spleen of zebrafish ( Danio rerio ). The results demonstrated that the inhibition of GSK-3β induced the mRNA expression of β-catenin and C/EBPα by lithium (Li) treatments or GSK-3β RNA interference. The levels of hydrogen peroxide (H 2 O 2 ), superoxide anion (O 2 .- ), and hydroxy radical (·OH) as well as the activity of superoxide dismutase (SOD) were increased, while the activities of catalase (CAT) and glutathione peroxidase (GSH-PX) were decreased in the spleen and ZF4 cells of zebrafish by Li + treatments. In addition, GSK-3β RNA interference increased ROS levels and decreased the activities of CAT and GSH-PX in the spleen. The fluorescence intensity of ROS was increased but the mitochondrial membrane potential (MMP) was decreased by Li + treatments in ZF4 cells labeled with 2′,7′-dichlorofluorescein diacetate (DCFH-DA) and Rhodamine-123, respectively. The results of present study indicated that the inhibition of GSK-3β promoted the ROS production via β-catenin/C/EBPα signaling in the spleen of zebrafish, and the balance between ROS and antioxidants could be destroyed by the GSK-3β/β-catenin/C/EBPα signaling. The results may be a valuable contribution to understanding the modulatory mechanism of GSK-3β/β-catenin/C/EBPα signaling on the antioxidant system in fish species. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10504648
- Volume :
- 76
- Database :
- Academic Search Index
- Journal :
- Fish & Shellfish Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 128945255
- Full Text :
- https://doi.org/10.1016/j.fsi.2018.02.040