Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line

Glycogen synthase kinase-3 (GSK-3) is an important immune regulator that controls inflammation via inhibition of its protein kinase activities. Persistent inflammatory responses through the activation of immune cells and excessive production of immune mediators may cause tissue destruction and impli...

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Main Authors: Zailan, Nur Fatin Zalikha, Jaganathan, Niranjana, Sandramuti, Thiban, Sarchio, Seri Narti Edayu, Hassan, Masriana
Format: Article
Language:English
Published: Faculty of Medicine and Health Sciences, University Putra Malaysia 2020
Online Access:http://psasir.upm.edu.my/id/eprint/89395/
http://psasir.upm.edu.my/id/eprint/89395/1/GLY.pdf
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author Zailan, Nur Fatin Zalikha
Jaganathan, Niranjana
Sandramuti, Thiban
Sarchio, Seri Narti Edayu
Hassan, Masriana
author_facet Zailan, Nur Fatin Zalikha
Jaganathan, Niranjana
Sandramuti, Thiban
Sarchio, Seri Narti Edayu
Hassan, Masriana
author_sort Zailan, Nur Fatin Zalikha
building UPM Institutional Repository
collection Online Access
description Glycogen synthase kinase-3 (GSK-3) is an important immune regulator that controls inflammation via inhibition of its protein kinase activities. Persistent inflammatory responses through the activation of immune cells and excessive production of immune mediators may cause tissue destruction and implicated in the development of chronic inflammatory diseases. The objective of this study was to examine the role of Tideglusib, a GSK-3 inhibitor, in inflammatory responses elicited through macrophage activation by investigating the expression of cell surface biomarkers and inflammatory molecule levels. Method: The effects of GSK-3 inhibition by Tideglusib on the expression of CD11b and CD40 and secretion of pro-inflammatory cytokines in the lipopolysaccharide (LPS)-activated macrophage-derived RAW 264.7 cells were determined by flow cytometry, while the presence of nitric oxide (NO) was determined by Griess assay. Results: Stimulation of RAW 264.7 cells with LPS increased substantial levels of CD11b and CD40 expressions, and secretion of NO, TNF-α, and MCP-1. However, the expression of these molecules was suppressed through inhibition of GSK-3. Conclusion: These findings suggest the significant role of Tideglusib to limit the upregulation of immune responses in activated macrophages, and as a potential anti-inflammatory drug for the intervention and treatment of inflammatory diseases.
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spelling upm-893952021-09-17T04:12:59Z http://psasir.upm.edu.my/id/eprint/89395/ Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line Zailan, Nur Fatin Zalikha Jaganathan, Niranjana Sandramuti, Thiban Sarchio, Seri Narti Edayu Hassan, Masriana Glycogen synthase kinase-3 (GSK-3) is an important immune regulator that controls inflammation via inhibition of its protein kinase activities. Persistent inflammatory responses through the activation of immune cells and excessive production of immune mediators may cause tissue destruction and implicated in the development of chronic inflammatory diseases. The objective of this study was to examine the role of Tideglusib, a GSK-3 inhibitor, in inflammatory responses elicited through macrophage activation by investigating the expression of cell surface biomarkers and inflammatory molecule levels. Method: The effects of GSK-3 inhibition by Tideglusib on the expression of CD11b and CD40 and secretion of pro-inflammatory cytokines in the lipopolysaccharide (LPS)-activated macrophage-derived RAW 264.7 cells were determined by flow cytometry, while the presence of nitric oxide (NO) was determined by Griess assay. Results: Stimulation of RAW 264.7 cells with LPS increased substantial levels of CD11b and CD40 expressions, and secretion of NO, TNF-α, and MCP-1. However, the expression of these molecules was suppressed through inhibition of GSK-3. Conclusion: These findings suggest the significant role of Tideglusib to limit the upregulation of immune responses in activated macrophages, and as a potential anti-inflammatory drug for the intervention and treatment of inflammatory diseases. Faculty of Medicine and Health Sciences, University Putra Malaysia 2020 Article PeerReviewed text en http://psasir.upm.edu.my/id/eprint/89395/1/GLY.pdf Zailan, Nur Fatin Zalikha and Jaganathan, Niranjana and Sandramuti, Thiban and Sarchio, Seri Narti Edayu and Hassan, Masriana (2020) Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line. Malaysian Journal of Medicine and Health Sciences, 16 (suppl. 9). pp. 2-8. ISSN 1675-8544 https://medic.upm.edu.my/upload/dokumen/2020110610495401_2020_0158.pdf
spellingShingle Zailan, Nur Fatin Zalikha
Jaganathan, Niranjana
Sandramuti, Thiban
Sarchio, Seri Narti Edayu
Hassan, Masriana
Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title_full Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title_fullStr Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title_full_unstemmed Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title_short Inhibition of GSK-3 by Tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated RAW 264.7 cell line
title_sort inhibition of gsk-3 by tideglusib suppresses activated macrophages and inflammatory responses in lipopolysaccharide-stimulated raw 264.7 cell line
url http://psasir.upm.edu.my/id/eprint/89395/
http://psasir.upm.edu.my/id/eprint/89395/
http://psasir.upm.edu.my/id/eprint/89395/1/GLY.pdf