Bcl‐2 hijacks the arsenic trioxide resistance in SH‐SY5Y cells

Wang, Jinling; Peng, Xiaohui; Yang, Daowei; Guo, Mengyu; Xu, Xiao Jie; Yin, Fengyue; Wang, Yu; Huang, Jie; Zhan, Linghui; Qi, Zhongquan

doi:10.1111/jcmm.17128

Cited by 6 publications

(1 citation statement)

References 24 publications

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“…HMGB1 (NBP2-62767, Novus), IFN-γ (CME0003, 4 A Biotech), IL-6 (CME0006, 4 A Biotech), and CXCL10 (CME0016, 4 A Biotech) concentrations in mouse serum were decided with enzyme-linked immunosorbent assay (ELISA, 4 A BIOTECH, China) kits according to the manufacturer’s instructions. The optical density of each sample was measured on an ELISA plate scanner (Multiskan Sky, Thermo Scientific, USA) at 450 nm [ 74 ].…”

Section: Methodsmentioning

confidence: 99%

Ketamine inhibits TNF-α-induced cecal damage by enhancing RIP1 ubiquitination to attenuate lethal SIRS

Deng

Yang

et al. 2022

Cell Death Discov.

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Systemic inflammatory response syndrome (SIRS) is a sepsis-associated inflammatory state and a self-defense mechanism against specific and nonspecific stimuli. Ketamine influences many key processes that are altered during sepsis. However, the underlying mechanisms remain incompletely understood. In this study, TNF-α-treated mice, as well as HT-29 and L929 cell models, were applied to characterize TNF-α-induced systemic and local cecal tissue inflammatory responses. Behavioral, biochemical, histological, and molecular biological approaches were applied to illustrate the related processes. Mice with TNF-α-induced SIRS showed systemic and local cecal tissue inflammatory responses, as indicated by increased levels of high mobility group box 1 protein (HMGB1), chemokines (C-X-C motif) ligand 10 (CXCL10), interleukin-6 (IL-6), and IL-10, as well as high mortality. Ketamine pretreatment alleviated death rates, symptoms, and the production of inflammatory cytokines induced by TNF-α in mice. Moreover, ketamine also protected the mice from TNF-α-induced cecal damage by suppressing the phosphorylation of receptor-interacting serine/threonine-protein kinase 3 (RIP3) and mixed lineage kinase domain-like protein (MLKL). In addition, our results showed that ketamine efficiently inhibited TNF-α-induced necroptosis in HT-29 and L929 cells. Furthermore, we explored the mechanism using different L929 cell lines. The results displayed that ketamine inhibited TNF-α-induced necroptosis by enhancing RIP1 ubiquitination and reducing the RIP1-RIP3 and RIP3-MLKL interactions, as well as the formation of necrosomes. Thus, our study may provide a new theoretical and experimental basis for treating diseases characterized by SIRS-associated inflammatory factor storms. Moreover, our exploration may provide potential molecular mechanisms and targets for therapeutic intervention and clinical application of ketamine.

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Section: Methodsmentioning

confidence: 99%