Silencing TLR4/MyD88/NF-κB Signaling Pathway Alleviated Inflammation of Corneal Epithelial Cells Infected by ISE

Wu, Liucheng; Du, Lili; Ju, Qianqian; Chen, Zhiheng; Ma, Yu; Bai, Ting; Ji, Guiqing; Wu, Yu; Liu, Zhaoguo; Shao, Yang; Peng, Xiaoqing

doi:10.1007/s10753-020-01363-1

Cited by 28 publications

(16 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activated TLR-4 in turns activates NF-κB signaling pathway 17 that eventually leads to the production and release of inflammatory cytokines (eg, TNF-α, IL1, and IL6). 24 , 45 , 46 MyD88 is an adaptor protein that plays a central role in TLR-4 signaling pathways. 47 TLR-4 recognizes pathogen-associated molecular patterns (PAMPs) and dimerizes with MyD88.…”

Section: Discussionmentioning

confidence: 99%

Network Pharmacology Analysis of the Mechanisms of Compound Herba Sarcandrae (Fufang Zhongjiefeng) Aerosol in Chronic Pharyngitis Treatment

Zhang

Yuan

et al. 2021

DDDT

View full text Add to dashboard Cite

Purpose This study aimed to investigate the molecular mechanisms of compound herba Sarcandrae aerosol, also known as the Fufang Zhongjiefeng (FFZJF) aerosol, in treating chronic pharyngitis (CP) using network pharmacology and in vivo experimental approaches. Methods Active compounds and putative targets of five herbs in FFZJF were identified from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, Chemistry Database, and Swiss Target Prediction databases. The therapeutic targets of CP were obtained from OMIM, Durgbank, DisGeNT, and GAD databases. The active compounds-target networks were constructed using Cytoscape 3.6.1. The overlapping targets of FFZJF active compounds and CP targets were further analyzed using the String database to construct protein–protein interaction (PPI) network. KEGG pathway and Gene Ontology enrichment analysis was performed using the Database for Annotation, Visualization, and Integrated Discovery. The predicted targets and pathways were validated in a group A β-hemolytic streptococcus-induced rat CP model. Results There were 45 active compounds identified from FFZJF and 11 potential protein targets identified for CP treatment. PPI network demonstrated that IL6, PTGS2, TLR-4, and TNF may serve as the key targets of FFZJF for the treatment of CP. The main functional pathways involving these key targets include cytokine secretion, inflammatory response, MyD88-dependent toll-like receptor signaling pathway, toll-like receptor signaling pathway, TNF signaling pathway, and NF-κB signaling pathway. In a rat CP model, the elevation of serum TNF-α, IL1β, and IL6 levels, as well as the upregulation of TLR-4, MyD88, NF-κB P65 in the pharyngeal mucosal tissues could be effectively reduced by FFZJF treatment in a dose-dependent manner. Conclusion Through a network pharmacology approach and animal study, we predicted and validated the active compounds of FFZJF and their potential targets for CP treatment. The results suggest that FFZJF can markedly alleviate GAS-induced chronic pharyngitis by modulating the TLR-4/MyD88/NF-κB signaling pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Network Pharmacology Analysis of the Mechanisms of Compound Herba Sarcandrae (Fufang Zhongjiefeng) Aerosol in Chronic Pharyngitis Treatment

Zhang

Yuan

et al. 2021

DDDT

View full text Add to dashboard Cite

show abstract

“…No reuse allowed without permission. TLR4/MyD88/NF-κB(p65) signal pathway activation has great significance in inflammation and fibrosis processes [16][17][18]. Some studies reveal ILK could effectively regulate this pathway [19].…”

Section: Discussionmentioning

confidence: 99%

ILK play a key role in partial bladder outler obstruction (PBOO) by regulation TLR4/NF-κB(p65) pathway

Zhou

Huang

Liu

et al. 2021

Preprint

View full text Add to dashboard Cite

AimThe purpose of this research was to discuss the effects and relative mechanisms of ILK in PBOO by vivo and vitro study.Materials and methodsThe SD rats were divided into Normal, Sham and Model groups. Collecting Bladder outlet tissue, observation pathology and fibrosis levels by H&E and Masson staining. Measuring cell apoptosis and cell viability by TUNEL and p-histone H3 staining, ILK protein were evaluated by WB and IHC assay in Bladder outlet tissue. Using TGF-β1 stimulating BSMC cell to make PBOO cell model. Measuring cell proliferation by CCK-8 assay; Relative gene and proteins expression were evaluated by immunofluorescence, WB and RT-qPCR assay.ResultsCompared with Normal group, bladder weight, collage fiber area, apoptosis cell number and cell viability were significantly difference with ILK protein significantly increasing in bladder outer tissues of Model group (P < 0.05, respectively). In vitro cell experiment, ILK overexpression had effects to stimulate cell proliferation via TLR4/NF-κB(p65) pathway; however, with ILK knockdown, the cell proliferation was significantly depressed via regulation TLR4/NF-κB(p65).ConclusionILK play an important role in PBOO induced cell proliferation, ILK knockdown had effects to improve PBOO induced cell hyper-proliferation via depressing TLR4/NF-κB(p65) pathway.

show abstract

“…It was reported that TLR4 silence could decrease inflammatory cytokines in corneal epithelial cells treated with inactivate staphylococcus epidermidis. 36 Blocking TLR4/MyD88/NF-κB signaling pathway may help reduce myocardial injury and improve cardiac function after coronary microembolization. 11 In order to confirm the hypothesis that blocking TLR4-MyD88-NF-κB signaling pathway could alleviate liver injury and fibrosis progression, we established an animal model of TLR4 knockout.…”

Section: Discussionmentioning

confidence: 99%

TLR4-MyD88-NF-κB signaling pathway contributes to the progression of secondary hepatic injury and fibrosis in hepatolithiasis

Fang

Zhou

et al. 2021

Eur J Inflamm

View full text Add to dashboard Cite

This paper focused on evaluating the effect of TLR4-MyD88-NF-κB signaling pathway in the progression of secondary hepatic injury and fibrosis in hepatolithiasis. The levels of inflammatory factors (IL-1β, IL-6, TNF-α) and serum biochemical values (ALT, AST, Tbil, Dbil, ALP, GGT) were detected by ELISA. IHC was used to detected the expression level of TLR4 in liver tissues of hepatolithiasis patients and mice. The pathological changes of liver tissue were observed by HE staining. The levels of MyD88, NF-κB, IκB, Laminin (LN), and chitosan enzyme 3-like protein 1 (CHI3L1) were detected by western blotting. In hepatolithiasis patients, the levels of TNF-α, IL-1β, and IL-6 were distinctly raised and proteins associated with TLR4-MyD88-NF-κB signaling pathway (such as TLR4, MyD88, NF-κB, and IκB) in liver tissues were significantly up-regulated. In Bile duct ligation (BDL) model of mice, the results showed that in addition to the significant increase of inflammatory factors, liver function indexes, and fibrosis indexes in BDL mice were also significantly up-regulated. Additionally, TLR4-MyD88-NF-κB signaling pathway was activated in BDL mice. After TLR4 knockdown in BDL mice, inflammatory factors, liver function indexes, and fibrosis indexes were significantly down-regulated. TLR4-MyD88-NF-κB signaling pathway proteins were restrained. TLR4-MyD88-NF-κB signaling pathway took part in the progression of secondary hepatic injury and fibrosis in hepatolithiasis. Inhibition of TLR4-MyD88-NF-κB signaling pathway can reduce the progression of secondary hepatic injury and fibrosis in hepatolithiasis.

show abstract

Silencing TLR4/MyD88/NF-κB Signaling Pathway Alleviated Inflammation of Corneal Epithelial Cells Infected by ISE

Cited by 28 publications

References 41 publications

Network Pharmacology Analysis of the Mechanisms of Compound Herba Sarcandrae (Fufang Zhongjiefeng) Aerosol in Chronic Pharyngitis Treatment

Network Pharmacology Analysis of the Mechanisms of Compound Herba Sarcandrae (Fufang Zhongjiefeng) Aerosol in Chronic Pharyngitis Treatment

ILK play a key role in partial bladder outler obstruction (PBOO) by regulation TLR4/NF-κB(p65) pathway

TLR4-MyD88-NF-κB signaling pathway contributes to the progression of secondary hepatic injury and fibrosis in hepatolithiasis

Contact Info

Product

Resources

About