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Anomalin attenuates LPS-induced acute lungs injury through inhibition of AP-1 signaling.

Abstract：

:In the present study, the anomalin was investigated to determine the protective effects and underlying mechanism against LPS-induced acute lung injury in mice. Anomalin administration 30 min after the LPS injection, significantly attenuated the mechanical allodynia, decrease body temperature, and improved the histological changes and inhibited the infiltration of leukocytes. The anomalin treatment markedly inhibited the production of pro-inflammatory mediators such as cytokines (IL-1β, IL-6 and TNF-α) and NO in contrast to the LPS treated groups. Similarly, the anomalin also enhanced the level of anti-oxidant enzymes such as GST, GSH, Catalase and inhibited oxidative stress marker such as MDA. In order to explore the molecular mechanism the effect of anomalin was evaluated for mitogen activated protein kinases (MAPK) in LPS-stimulated RAW264.7 cells. The anomalin treatment significantly attenuated the MAPK proteins such as ERK1/2, JNK and p38 (which is downstream signaling proteins to the MAPKKKs and MAPKKs protein) in the RAW264.7 macrophages using western blot analysis. Furthermore, the western blot analysis showed that anomalin treatment significantly inhibited the activation of the Akt proteins in the RAW264.7 macrophages. The AP-1 served as downstream target for the MAPK pathways and the blocking MAPK pathways is responsible for the inhibition of the AP-1 protein. The AP-1/DNA binding was assessed in the RAW264.7 cells using EMSA. The anomalin treatment significantly restricted the AP-1/DNA binding activity and the decrease in the AP-1/DNA binding activity might be contributed due to the upstream inhibition of the MAPKs signaling.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Khan A,Khan S,Ali H,Shah KU,Ali H,Shehzad O,Onder A,Kim YS

doi

10.1016/j.intimp.2019.05.032

subject

Has Abstract

pub_date

2019-08-01 00:00:00

pages

451-460

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)30663-0

journal_volume

73

pub_type

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