The Role of Erbin in GTS-21 Regulating Inflammtory Responses in MDP-Stimulated Macrophages

The Role of Erbin in GTS-21 Regulating Inflammtory Responses in MDP-Stimulated Macrophages
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DOI:
10.1097/shk.0000000000000785
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发表时间:
2017-05
期刊:
影响因子:
3.1
通讯作者:
Xiao-jing Wu;Xu-Ming Yang;Xuemin Song;Yang Xu;Jian-guo Li;Yanlin Wang;Zongze Zhang;Lin-Li Le;Hui Liang;Yin B. Zhang
Xiao-jing Wu;Xu-Ming Yang;Xuemin Song;Yang Xu;Jian-guo Li;Yanlin Wang;Zongze Zhang;Lin-Li Le;Hui Liang;Yin B. Zhang
中科院分区:
医学2区
文献类型:
--
作者:
Xiao-jing Wu;Xu-Ming Yang;Xuemin Song;Yang Xu;Jian-guo Li;Yanlin Wang;Zongze Zhang;Lin-Li Le;Hui Liang;Yin B. Zhang

文献摘要

相似文献

Objective: To explore the role of Erbin protein and nucleotide-binding oligomerization domain 2/receptor-interacting serine/threonine protein kinases (NOD2/RICK) in GTS-21 activating cholinergic anti-inflammatory pathway. Methods: Experiments were randomly divided into four groups: normal control (NC) group, muramyl dipeptide (MDP) group, 10 g/mL MDP, GTS-21 (GTS) group, 10 g/mL MDP plus 50 g/mL GTS-21 (7 nAChRs agonist), Erbin shRNA interference (sh-Erbin) group: sh-Erbin RNA plus 10 g/mL MDP and 50 g/mL GTS-21. We extract specimens at the point of 1, 6, and 24 h after stimulation of MDP in Raw264.7 macrophages. Results: After stimulation of MDP, the NLR2 mRNA, RICK and Erbin protein, nuclear factor (NF)-B activity, the pro-inflammatory cytokines tumor necrosis factor (TNF)- and HMGB1 were significantly increased in MDP group (P <0.05). The expression peak of TNF- is at 1 h. The peak of HMGB1 is at 24 h. Compared with MDP group, the NLR2 mRNA, RICK, NF-B, TNF-, and HMGB1 were significantly decreased, but the Erbin was increased in GTS group (P <0.05). Compared with GTS group, the NLR2 mRNA, RICK, NF-B, TNF-, and HMGB1 increase in sh-Erbin group (P <0.05). Conclusion: GTS-21 could significantly inhibit MDP-induced pro-inflammatory cytokines responses via activating cholinergic anti-inflammatory pathway, and the Erbin might be the key negative regulatory protein in NLR2/RICK signal transduction.