Inula japonica ameliorated the inflammation and oxidative stress in LPS-induced acute lung injury through the MAPK/NF-κB and Keap1/Nrf2 signalling pathways

Author:

Zhang Min12,Zhang Juan13,Zhu Qi-Meng1,Zhao Wen-Yu1,Lv Xia1,Yi Jing1,Huo Xiao-Kui1,Wang Mi-Jia2,Sun Cheng-Peng1

Affiliation:

1. College of Pharmacy, College (Institute) of Integrative Medicine, Dalian Medical University , Dalian , China

2. Second Affiliated Hospital, Dalian Medical University , Dalian , China

3. School of Pharmaceutical Sciences, Health Science Center, Shenzhen University , Shenzhen , China

Abstract

Abstract Objectives To investigate the protective effect and underlying mechanism of Inula japonica (TEIJ) in the treatment of acute lung injury (ALI). Methods Protective effects of TEIJ in the inflammation and oxidative stress were studied in lipopolysaccharide (LPS)-induced ALI mice. Meanwhile, Western blot and real-time qPCR were carried out to investigate the underlying mechanism of TEIJ for ALI as well as immunohistochemistry. Key findings TEIJ significantly alleviated the course of ALI via suppressing the interstitial infiltrated inflammatory cells, the increase of inflammatory factors and the decrease of anti-oxidative factors. TEIJ inactivated the MAPK/NF-κB signalling pathway to suppress the transcription of its downstream target genes, such as TNF-α, IL-6, etc. Meanwhile, TEIJ activated the Keap1/Nrf2 signalling pathway to regulate expression levels of Nrf2 and its target proteins. The results of LC-QTOF-MS/MS indicated potential active constituents of I. japonica, terpenoids and flavonoids. Additionally, terpenoids and flavonoids synergistically alleviated LPS-induced ALI depending on MAPK/NF-κB and Keap1/Nrf2 signalling pathways. Conclusion I. japonica could be considered a potential agent to treat ALI via regulating the MAPK/NF-κB and Keap1/Nrf2 signalling pathways.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Liaoning Province

Dalian Young Star of Science and Technology

Publisher

Oxford University Press (OUP)

Subject

Pharmaceutical Science,Pharmacology

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