Language:

Dexmedetomidine attenuates subarachnoid hemorrhage-induced acute lung injury through regulating autophagy and TLR/NFκB signaling pathway

Korean journal of anesthesiology, 2022-12, Vol.75 (6), p.518-529 [Peer Reviewed Journal]

Copyright © The Korean Society of Anesthesiologists, 2022 2022 ;ISSN: 2005-6419 ;EISSN: 2005-7563 ;DOI: 10.4097/kja.22165 ;PMID: 35912428

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
Dexmedetomidine attenuates subarachnoid hemorrhage-induced acute lung injury through regulating autophagy and TLR/NFκB signaling pathway
Author: Han, Dong Woo ; Oh, Ju Eun ; Lim, Beom Jin ; Han, Yeonseung ; Song, Young
Subjects: acute lung injury ; Acute Lung Injury - complications ; Acute Lung Injury - prevention & control ; Animals ; Autophagy ; dexmedetomidine ; Dexmedetomidine - pharmacology ; Experimental ; inflammation ; Interleukin-6 - therapeutic use ; Male ; NF-kappa B - metabolism ; Pulmonary Edema - complications ; Pulmonary Edema - prevention & control ; Rats ; Rats, Wistar ; Signal Transduction ; subarachnoid hemorrhage ; Subarachnoid Hemorrhage - complications ; Subarachnoid Hemorrhage - drug therapy ; Toll-Like Receptor 4 - metabolism ; Toll-Like Receptor 9 - metabolism ; toll-like receptors
Is Part Of: Korean journal of anesthesiology, 2022-12, Vol.75 (6), p.518-529
Description: Acute lung injury (ALI) is the most serious complication of subarachnoid hemorrhage (SAH). We investigated role of autophagy and inflammatory signaling pathways in lung damage and therapeutic effects of dexmedetomidine (DEX). Fifty male Wistar rats were randomly divided into five groups: sham, SAH, SAH+ DEX5, SAH+DEX25, and SAH+DEX50. SAH was induced using endovascular perforation technique. All rats received mechanical ventilation for 60 minutes. At 2 and 24 h of SAH induction, SAH+DEX groups were treated with 5, 25, and 50 µg/kg of DEX, respectively. Histological ALI score and pulmonary edema were assessed after 48 h. Lung expression of LC3B, ATG3, p62, TLR4, TLR9, and NFκB was assessed using western blotting and quantitative PCR. Blood levels of IL-6, IL-1β, IFN-γ, and TNFα were also assessed. SAH induced ALI and pulmonary edema, which were attenuated in SAH+DEX5 (P < 0.001 for both) and SAH+DEX25 groups (P = 0.001 and P < 0.001 for ALI and edema, respectively). Lung expressions of LC3B and ATG3 were upregulated in SAH group, which was attenuated in SAH+DEX5 and SAH+DEX25 groups. Lung expressions of TLR4, TLR9, and NFκB were increased in SAH group, which was attenuated in SAH+DEX5 group. Blood IL-6 level was increased in SAH group and attenuated in SAH+DEX5 and SAH+DEX25 groups. Blood IFN-γ level was lower in SAH group than in sham group, and it was increased in SAH+DEX25 group. Low-dose DEX treatment after SAH may protect against ALI by disrupting pathological brain-lung crosstalk and alleviating autophagy flux and TLR-dependent inflammatory pathways.
Publisher: Korea (South): Korean Society of Anesthesiologists
Language: English
Identifier: ISSN: 2005-6419
EISSN: 2005-7563
DOI: 10.4097/kja.22165
PMID: 35912428
Source: KoreaMed Synapse
MEDLINE
PubMed Central
KoreaMed Open Access
DOAJ Directory of Open Access Journals

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

Dexmedetomidine attenuates subarachnoid hemorrhage-induced acute lung injury through regulating autophagy and TLR/NFκB signaling pathway

Copyright © The Korean Society of Anesthesiologists, 2022 2022 ;ISSN: 2005-6419 ;EISSN: 2005-7563 ;DOI: 10.4097/kja.22165 ;PMID: 35912428

Searching Remote Databases, Please Wait