| Literature DB >> 31522340 |
Xin Zhao1,2, Zhizhong Yu1,2, Zheng Lv1,2, Lei Meng1,2, Jiaxin Xu1,2, Shiying Yuan1,2, Zhaohui Fu3,4.
Abstract
The release of inflammatory cytokines and chemokines and autophagy has been reported to be involved in the pathogenic mechanism of acute lung injury (ALI). Reportedly, alpha-7 nicotinic acetylcholine receptors (α7nAchR) might play a protective role in LPS-induced ALI. In the current research, we established LPS-induced ALI model in mice and α7nAchR agonist PNU-282987 improved LPS-induced injury. In MH-S cells, LPS stimulation inhibited, whereas α7nAchR agonist PNU-282987 enhanced the autophagy. α7nAchR agonist PNU-282987 protected MH-S cells from LPS-induced inflammation by reducing the concentrations of IL-6, TNF-α, and IL-1β. Finally, LPS stimulation dramatically inhibited MH-S cell viability but enhanced cell apoptosis, whereas PNU-282987 treatment exerted opposite effects; α7nAchR might regulate the cellular homeostasis via affecting the crosstalk between the autophagy and apoptosis in MH-S cells; in other words, α7nAChR agonist enhances MH-S cell autophagy and inhibits MH-S cell apoptosis. In conclusion, α7nAchR promote the protective autophagy in LPS-induced ALI model in mice and MH-S cells. The application of α7nAchR agonist is considered a potent target for LPS-induced ALI, which needs further clinical investigation.Entities:
Keywords: acute lung injury (ALI); alpha-7 nicotinic acetylcholine receptors (α7nAchR); apoptosis; autophagy
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Year: 2019 PMID： 31522340 DOI： 10.1007/s10753-019-01088-w
Source DB: PubMed Journal: Inflammation ISSN： 0360-3997 Impact factor: 4.657