Bibliographic Details
Title: |
Lomerizine attenuates LPS-induced acute lung injury by inhibiting the macrophage activation through reducing Ca2+ influx |
Authors: |
Yunduan Song, Yusen Gou, Jiameng Gao, Dongxin Chen, Haibo Zhang, Wenjuan Zhao, Feng Qian, Ajing Xu, Yao Shen |
Source: |
Frontiers in Pharmacology, Vol 14 (2023) |
Publisher Information: |
Frontiers Media S.A., 2023. |
Publication Year: |
2023 |
Collection: |
LCC:Therapeutics. Pharmacology |
Subject Terms: |
lomerizine, acute lung injury, calcium, macrophage, cytokine, inflammation, Therapeutics. Pharmacology, RM1-950 |
More Details: |
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening lung diseases with high mortality rates, predominantly attributable to acute and severe pulmonary inflammation. Lomerizine (LMZ) is a calcium channel blocker previously used in preventing and treating migraine. Here, we found that LMZ inhibited inflammatory responses and lung pathological injury by reducing pulmonary edema, neutrophil infiltration and pro-inflammatory cytokine production in lipopolysaccharide (LPS)-induced ALI mice. In vitro experiments, upon treating with LMZ, the expression of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was attenuated in macrophages. The phosphorylation of p38 MAPK, ERK1/2, JNK, and NF-κB p65 was inhibited after LMZ treatment. Furthermore, LPS-induced Ca2+ influx was reduced by treating with LMZ, which correlated with inhibition of pro-inflammatory cytokine production. And L-type Ca2+ channel agonist Bay K8644 (BK) could restore cytokine generation. In conclusion, our study demonstrated that LMZ alleviates LPS-induced ALI and is a potential agent for treating ALI/ARDS. |
Document Type: |
article |
File Description: |
electronic resource |
Language: |
English |
ISSN: |
1663-9812 |
Relation: |
https://www.frontiersin.org/articles/10.3389/fphar.2023.1236469/full; https://doaj.org/toc/1663-9812 |
DOI: |
10.3389/fphar.2023.1236469 |
Access URL: |
https://doaj.org/article/30fa29fee8514efd979f555683ccabe1 |
Accession Number: |
edsdoj.30fa29fee8514efd979f555683ccabe1 |
Database: |
Directory of Open Access Journals |