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NLM348466986 |
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DE-627 |
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20250304014447.0 |
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231226s2022 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2022.109169
|2 doi
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|a pubmed25n1161.xml
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|a (DE-627)NLM348466986
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|a (NLM)36332815
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|a (PII)S1521-6616(22)00250-9
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Liu, WenJun
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Cyclic helix B peptide ameliorated the sepsis-induced injury in human HPMEC cells through regulating NF-κB
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|c 2022
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 25.11.2022
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|a Date Revised 26.12.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2022. Published by Elsevier Inc.
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|a BACKGROUND: Sepsis is a life-threatening condition. The incidence of severe sepsis is increasing. Sepsis is often complicated with organ dysfunctions. Cyclic helix B peptide (CHBP) is a peptide derivant of erythropoietin with powerful tissue-protective efficacies. However, the role of CHBP in sepsis-induced injury remains unclear
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|a MATERIAL AND METHODS: Lyso-phosphatidylserine (LPS) was used to induce sepsis in human pulmonary microvascular endothelial cells (HPMECs). Cell growth was detected using Cell Counting Kit-8. Cell permeability was measured using fluorescein isothiocyanate (FITC)-dextran. Cecal ligation and puncture (CLP) method was applied to induce sepsis and CHBP was provided to test its efficacy. Western blot assays were used to evaluate gene expression
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|a RESULTS: Administration of CHBP ameliorated LPS-induced injury in HPMECs dose-dependently. Administration of CHBP decreased the permeability of LPS-treated HPMEC cells in a same way as well. Furthermore, we identified that recombinant CHBP protein (Re-CHBP) ameliorated CLP-induced injury in vivo. Finally, we found that administration of NF-κB activator, TNF-α, abolished the function of Re-CHBP in LPS-treated HPMEC cells
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|a CONCLUSION: CHBP ameliorated sepsis-induced injury dose dependently both in vitro and in vivo through decreasing the permeability of HPMEC cells via suppressing NF-κB signaling and inflammation. Present findings highlight the importance of CHBP/NF-κB signaling in septic injury and provide new insights into therapeutic strategies for sepsis-induced injury
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Cell permeability
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|a Cyclic helix B peptide
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|a Inflammation
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|a NF-κB activation
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| 650 |
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|a sepsis
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| 650 |
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|a NF-kappa B
|2 NLM
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| 650 |
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|a Lipopolysaccharides
|2 NLM
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| 650 |
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7 |
|a Peptides, Cyclic
|2 NLM
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| 700 |
1 |
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|a Huang, DanLei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, YuJing
|e verfasserin
|4 aut
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| 700 |
1 |
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|a He, HongYu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gu, ZhunYong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Liu, YiMei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Yang, QingNan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Luo, Zhe
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ju, MinJie
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 245(2022) vom: 24. Dez., Seite 109169
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnas
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| 773 |
1 |
8 |
|g volume:245
|g year:2022
|g day:24
|g month:12
|g pages:109169
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2022.109169
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|h 109169
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