Nicotine plays a protective role in rats with induced viral pneumonia with polyinosinic-polycytidylic acid through α7nAChR.
Cholinergic anti-inflammatory pathway
Nicotine
Pneumonia
Poly (I:C)
Rats
Journal
Heliyon
ISSN: 2405-8440
Titre abrégé: Heliyon
Pays: England
ID NLM: 101672560
Informations de publication
Date de publication:
Nov 2023
Nov 2023
Historique:
received:
22
03
2023
revised:
25
10
2023
accepted:
25
10
2023
medline:
29
11
2023
pubmed:
29
11
2023
entrez:
29
11
2023
Statut:
epublish
Résumé
To study the effect of nicotine in rat model of pneumonia induced by polyinosinic-polycytidylic acid [Poly (I:C)] and explore the underlying mechanism. Twenty-four healthy adult male Sprague-Dawley (SD) rats (200-250 g) were randomly divided into normal saline control group (NS group); Poly (I:C) group; nicotine group (NIC group); and α7 nicotinic acetylcholine receptor (α7nAChR) antagonist group (α-BGT group) (n = 6 each). Rats in the Poly (I: C), NIC, and α-BGT groups were administered 1.5 mg/mL 100 μL Poly (I:C) intranasally to establish pneumonia model. In α-BGT group, 1 μg/kg α-bungarotoxin (α-BGT) was intraperitoneally injected 45 min before intranasal Poly (I:C), and 400 μg/kg nicotine was intraperitoneally injected 15 min after α-BGT injection. The NIC group received an equal volume of NS in place of α-BGT while the other treatments were same. The Poly (I:C) group received equal volume of NS in place of nicotine while the other treatments were same as in NIC group. In the NS group, only NS was administered at all three time points. PaCO Compared with NS group, Poly (I:C) and α-BGT groups showed significantly increased W/D ratio, PaCO Pre-administration of nicotine improved Poly (I:C)-induced pneumonia by activating the cholinergic anti-inflammatory pathway.
Identifiants
pubmed: 38027680
doi: 10.1016/j.heliyon.2023.e21667
pii: S2405-8440(23)08875-8
pmc: PMC10656239
doi:
Types de publication
Journal Article
Langues
eng
Pagination
e21667Informations de copyright
© 2023 Published by Elsevier Ltd.
Déclaration de conflit d'intérêts
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Références
Respir Res. 2009 Jun 01;10:43
pubmed: 19486528
Eur Respir J. 2020 Jul 16;56(1):
pubmed: 32444400
FEBS J. 2022 Feb;289(4):883-900
pubmed: 33624419
Crit Care Med. 2022 Sep 1;50(9):e696-e706
pubmed: 35191411
Arch Toxicol. 2011 Jun;85(6):663-8
pubmed: 21337027
Am J Respir Crit Care Med. 2017 Mar 15;195(6):725-736
pubmed: 28040987
Sci Rep. 2021 Jun 4;11(1):11886
pubmed: 34088975
Nature. 2020 Aug;584(7821):463-469
pubmed: 32717743
Nature. 2000 May 25;405(6785):458-62
pubmed: 10839541
Am J Respir Cell Mol Biol. 2011 May;44(5):725-38
pubmed: 21531958
Cell Death Dis. 2021 Jan 7;12(1):53
pubmed: 33414457
Mol Med. 2020 Jun 29;26(1):64
pubmed: 32600316
Nature. 2021 Mar;591(7848):92-98
pubmed: 33307546
DNA Cell Biol. 2005 Oct;24(10):614-23
pubmed: 16225392
Neurochem Res. 2018 Jun;43(6):1269-1282
pubmed: 29737480
Mol Pharmacol. 2013 Jan;83(1):61-72
pubmed: 23028093
Front Immunol. 2017 Sep 06;8:1085
pubmed: 28932225
Sci Rep. 2022 Jan 7;12(1):54
pubmed: 34997096
Nature. 2003 Jan 23;421(6921):384-8
pubmed: 12508119
Inflammation. 2011 Aug;34(4):231-7
pubmed: 20625922
Infection. 2021 Aug;49(4):607-616
pubmed: 33782861
Cell. 2021 Jan 7;184(1):149-168.e17
pubmed: 33278357
Science. 2020 Aug 7;369(6504):718-724
pubmed: 32661059
Neurotox Res. 2020 Oct;38(3):665-681
pubmed: 32767216
FEBS J. 2020 Sep;287(17):3656-3663
pubmed: 32790936