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Synergism Between Taurine and Dexamethasone in Anti-inflammatory Response in LPS-Activated Macrophages.
Do, Chang-Hee; Lee, Dong-Hee.
Afiliação
  • Do CH; Department of Animal Biosystem Science, College of Agriculture and Life Science, Chungnam National University, Daejeon, South Korea.
  • Lee DH; Department of Life Sciences, University of Seoul, Seoul, South Korea. leedh@uos.ac.kr.
Adv Exp Med Biol ; 1370: 31-39, 2022.
Article em En | MEDLINE | ID: mdl-35882779
The aim of the present study is to examine the potential effect of dexamethasone (DEX) and taurine (TAU) on endoplasmic reticular stress (ERS) and inflammation. The macrophages were pre-treated with DEX or TAU, and the level of ERS and pro-inflammatory response was evaluated in LPS-activated macrophages. The expression of ERS marker proteins (GRP78 and CHOP) and the pro-inflammatory cytokines (IL-1ß and IL-6) was analyzed by immunoblotting and ELISA of LPS-induced macrophages. At lower concentrations (<50 nM), DEX alone reduced the levels of ERS and pro-inflammatory markers. Similarly, TAU reduced the expression of LPS-induced ERS and pro-inflammatory markers. When treated with a combination of DEX and TAU, however, the macrophages showed even a greater level of reduction in ERS and pro-inflammatory responses. The RT-qPCR data indicate that the reduction of ERS markers is caused by the inhibition of their own transcriptional expression. The significant level of reduction can be interpreted as a strong synergistic effect (p < 0.01). In summary, the results strongly indicate that a single pre-treatment of DEX or TAU may attenuate ERS and inflammation in LPS-induced macrophages at the concentrations tested in this study. Most importantly, concurrent treatment of macrophages by both agents reduced the level of ERS and pro-inflammatory cytokines in a synergistic fashion.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Humans Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Limite: Humans Idioma: En Ano de publicação: 2022 Tipo de documento: Article