Open AccessGSK-3β Inhibition Attenuates LPS-Induced Death but Aggravates Radiation-Induced Death via Down-Regulation of IL-6
Author(s) -
Bailong Li,
Chaoxiong Zhang,
Feng He,
Wen Liu,
Yanyong Yang,
Liu Hu,
Xin Liu,
Jie Wang,
Lin Zhang,
Bo Deng,
Fu Gao,
Jianguo Cui,
Cong Liu,
Jianming Cai
Publication year - 2013
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000356606
Subject(s) - programmed cell death , apoptosis , tlr4 , necroptosis , biology , inflammation , tumor necrosis factor alpha , gsk 3 , immune system , viability assay , lipopolysaccharide , annexin , signal transduction , cancer research , microbiology and biotechnology , immunology , biochemistry
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.
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