Study on Mechanism of Linggan Wuwei Jiangxintang in Treating Acute Lung Injury
10.13422/j.cnki.syfjx.20231215
- VernacularTitle:苓甘五味姜辛汤治疗急性肺损伤的作用机制
- Author:
Quanwu DAI
1
;
Yi LIU
1
;
Gege ZENG
1
;
Jiawei HE
1
;
Zhenyang HUANG
1
Author Information
1. Hubei Medicinal Plant Research and Development Center， Hubei University of Chinese Medicine， Wuhan 430065， China
- Publication Type:Journal Article
- Keywords:
Linggan Wuwei Jiangxintang;
acute lung injury;
inflammation;
Toll-like receptor 4（TLR4）/nuclear transcription factor（NF）-κB signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(24):95-103
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the action mechanism of Linggan Wuwei Jiangxintang on the treatment of lipopolysaccharide （LPS）-induced acute lung injury （ALI） in mice. MethodTraditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）， GeneCards， DisGeNET， and Herb databases were combined with clinical data from Gene Expression Omnibus （GEO） to screen the key targets of Linggan Wuwei Jiangxintang in the treatment of ALI. The protein-protein interaction （PPI） network was constructed to screen the core targets， and gene ontology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） pathway enrichment analyses were performed. The mouse ALI model was established by LPS induction to verify the effect and key targets of Linggan Wuwei Jiangxintang on the treatment of ALI. The expression levels of Toll-like receptor 4 （TLR4）， nuclear transcription factor-κB p65 （NF-κB p65）， and phosphorylated NF-κB p65 （NF-κB p-p65） in lung tissue were detected by Western blot. ResultThe analysis showed that the treatment of ALI with Linggan Wuwei Jiangxintang was related to 10 core targets such as interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and JUN， involving TNF signaling pathway， Toll-like receptor signaling pathway， NF-κB signaling pathway， etc. The animal experimental results show that Linggan Wuwei Jiangxintang can reduce lung injury， improve the pathological state of ALI mice， significantly reduce the expression of TNF-α and IL-6 in serum， increase the activity of total superoxide dismutase （T-SOD） and catalase （CAT） in lung tissue， and reduce the expression levels of JUN， TLR4， NF-κB p65， and NF-κB p-p65 proteins in lung tissue. ConclusionLinggan Wuwei Jiangxintang can inhibit LPS-induced inflammation and oxidative damage in ALI mice， and its mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway and the reduction of inflammatory factors such as TNF-α and IL-6.
