GSK-3β inhibition attenuates LPS-induced death but aggravates radiation-induced death via down-regulation of IL-6

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
Bailong LiJianming Cai

Abstract

Exposure of high dose ionizing radiation is lethal. Signal pathways involved in radiation biology reaction still remain illdefined. Lipopolysaccharides (LPS), the ligands of Toll-like receptor 4(TLR4), could elicit strong immune responses. Glycogen synthase kinase-3β(GSK-3β) promotes the production of inflammatory molecules and cell migration. Inhibition of GSK-3β provides protection against inflammation in animal models. The aim of the study was to investigate role of GSK-3β in LPS shock and ionizing radiation. WT or IL-6(-/-)mice or cells were pretreated with SB216763, a GSK-3β inhibitor, and survival of the mice was determined. Cell viability was assayed by Cell Counting Kit. Apoptosis was assayed by Annexin V-PI double staining. Serum concentrations of IL-6 and TNF-α were determined by ELISA. SB216763 attenuated LPS induced mice or cell death but aggravated radiation induced mice or cell death. SB216763 reduced IL-6, but not TNF-α levels in vivo. IL-6(-/-) mice were more resistant to LPS-induced death but less resistant to radiation-induced death than wild type mice. Inhibition of GSK-3β conferred resistance to LPS shock but fostered death induced by ionizing radiation. Inhibition of GSK-3β was effective by reducing IL-6.

Citations

Mar 7, 2014·Antioxidants & Redox Signaling·Nidhi BansalCristina M Furdui
Apr 1, 2016·Medical Science Monitor : International Medical Journal of Experimental and Clinical Research·Haiyan ZhouLong Li
May 22, 2021·Frontiers in Immunology·Ricarda Cortés-VieyraVíctor M Baizabal-Aguirre

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