Quercetin Inhibits the Production of IL-1β-Induced Inflammatory Cytokines and Chemokines in ARPE-19 Cells via the MAPK and NF-κB Signaling Pathways

Cheng, Shu-Chen; Huang, Wen‐Chung; Pang, Jong‐Hwei S.; Wu, Yijing; Cheng, Ching‐Yi

doi:10.3390/ijms20122957

Cited by 173 publications

(103 citation statements)

References 92 publications

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“…These findings indicated that the JNK1/2 signaling pathway had nothing to do with expression of MCP-1, sICAM-1, sVCAM-1, ICAM-1, and VCAM-1. Some of these observations are identical to the findings reported by Bian et al and Cheng et al, who showed that only ERK1/2 or p38 inhibitors were able to reduce sICAM-1 and MCP-1 levels [30,31]. We believe that this conclusion provides more precise targets for the intervention of monocyte-endothelial adherence.…”

Section: Mediators Of Inflammationsupporting

confidence: 90%

Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells

Chai

Liu

et al. 2020

Mediators of Inflammation

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Current studies have identified the multifaceted protective functions of dexmedetomidine on multiple organs. For the first time, we clarify effects of dexmedetomidine on monocyte-endothelial adherence and whether its underlying mechanism is relative to connexin43 (Cx43), a key factor regulating monocyte-endothelial adherence. U937 monocytes and human umbilical vein endothelial cells (HUVECs) were used to explore monocyte-endothelial adherence. Two special siRNAs were designed to knock down Cx43 expression on HUVECs. U937-HUVEC adhesion, adhesion-related molecules, and the activation of the MAPK (p-ERK1/2, p-p38, and p-JNK1/2) signaling pathway were detected. Dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), was given as pretreatments to HUVECs. Its effects on Cx43 and U937-HUVEC adhesion were also investigated. The results show that inhibiting Cx43 on HUVECs could attenuate the contents of MCP-1, soluble ICAM-1 (sICAM-1), soluble VCAM-1 (sVCAM-1), and the nonprocessed variants of the adhesion molecules ICAM-1 and VCAM-1 and ultimately result in U937-HUVEC adhesion decrease. Meanwhile, the activation of MAPKs was also inhibited. U0126 (inhibiting p-ERK1/2) and SB202190 (inhibiting p38) decreased the contents of MCP-1, sICAM-1, and sVCAM-1, but SP600125 (inhibiting p-JNK1/2) had none of these effects. ICAM-1 and VCAM-1 could be regulated in a similar way. Dexmedetomidine pretreatment inhibited Cx43 on HUVECs, the activation of MAPKs, and U937-HUVEC adhesion. Therefore, we conclude that dexmedetomidine attenuates U937-HUVEC adhesion via inhibiting Cx43 on HUVECs modulating the activation of MAPK signaling pathways.

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Section: Mediators Of Inflammationsupporting

confidence: 90%

Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells

Chai

Liu

et al. 2020

Mediators of Inflammation

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“…On the other hand, under the stimulation of inflammatory mediators, such as tumor necrosis factor (TNF)-α, interferon (IFN)-γ and interleukin (IL)-1β, RPE cells produce cytokines and chemokines, including IL-4, -5, -6, -8, -10, -13, -17, IFN-β, IFN-γ, TGF-β, MCP-1 and VEGF. The interaction of pro-inflammatory and anti-inflammatory cytokines ultimately leads to chronic inflammatory responses [39,40]. Inflammatory cytokines can also enhance the secretion of VEGF, which can initiate and cause the pathological CNV and retinal neovascularization of AMD, and macrophages and lymphocytes were found in the active CNV stage [41].…”

Section: Inflammation In Amd Pathogenesismentioning

confidence: 99%

The Role of Inflammation in Age-Related Macular Degeneration

Tan¹,

Zou²,

Yoshida³

et al. 2020

Int. J. Biol. Sci.

146

103

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Age-related macular degeneration (AMD) is a blinding eye disease which incidence gradually increases with age. Inflammation participates in AMD pathogenesis, including choroidal neovascularization and geographic atrophy. It is also a kind of self-protective regulation from injury for the eyes. In this review, we described inflammation in AMD pathogenesis, summarized the roles played by inflammation-related cytokines, including pro-inflammatory and anti-inflammatory cytokines, as well as leukocytes (macrophages, dendritic cells, neutrophils, T lymphocytes and B lymphocytes) in the innate or adaptive immunity in AMD. Possible clinical applications such as potential diagnostic biomarkers and anti-inflammatory therapies were also discussed. This review overviews the inflammation as a target of novel effective therapies in treating AMD.

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“…Cytokine storm, emerged from prolonged cytokine/chemokine responses during COVID-19, causes ARDS or multiple-organ dysfunction, ultimately leading to physiological deterioration and death [30]. Quercetin, a typical avonoid, is one of the major compounds of FF, LIF, EH, HH, PCB, and LI in LHQW capsule and has been reported to have the effects of anti-in ammation, antiviral, strengthening the endothelial barrier integrity and inhibiting the expression of cytokines [31][32][33][34]. Kaempferol is avonoid found in FF, LIF, EH, FBR, HH, and LI of LHQW capsule, and can protect against in ammation, virus infection, endothelial barrier dysfunction, and cytokines release [35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

Exploring the Mechanisms of Lian Hua Qing Wen Capsule against COVID-19 by Network Pharmacology and Molecular Docking Approach

Chen¹,

Qu²,

Tan³

et al. 2020

Preprint

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Background The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or COVID-19) disease has led to a wide-spread global pandemic. There is no specific antiviral drug proven effective for the treatment of patients with COVID-19 at present. Combination of western and traditional Chinese medicine (TCM) is recommended, and Lian Hua Qing Wen (LHQW) capsule is a basic prescription and widely used to treat COVID-19 in China. However, the mechanisms of LHQW capsule treating COVID-19 are not clear. The aim of the study is to explore the mechanisms of LHQW capsule treating COVID-19 based on network pharmacy and molecular docking approach. Methods The active compounds and targets of LHQW capsule were obtained from traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP). COVID-19 related target genes were obtained from GeneCards database and OMIM database. Protein–protein interaction (PPI) networks of LHQW capsule targets and COVID-19-related genes were visualized and merged to identify the candidate targets for LHQW capsule treating COVID-19. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were also performed. The hub genes involved in the gene-related pathways were screened and their corresponding compounds were used for in vitro validation of molecular docking predictions.Results A total of 185 active compounds of LHQW capsule were screened out, and 263 targets were predicted. Third hundred and fifty-two COVID-19 related target genes were obtained from GeneCards database and OMIM database. GO functional enrichment analysis showed that the biological processes of LHQW capsule treating COVID-19 were closely linked with the regulation of inflammation, immunity, cytokines production, vascular permeability, oxidative stress and apoptosis. KEGG enrichment analysis revealed that the pathways of LHQW capsule treating COVID-19 were significantly enriched in AGE−RAGE signaling pathway in diabetic complications, Kaposi sarcoma−associated herpesvirus infection, TNF, IL−17, and Toll−like receptor (TLR) signaling pathway. The hub targets genes in the gene-related pathways analysis of LHQW capsule treating COVID-19 included MAPK1, MAPK3, RELA, IL-6 and CASP8, which closely associated with inflammation, cytokines storm and apoptosis. Finally, molecular docking showed that top 5 compounds of LHQW capsule also had good binding activities to the important targets in COVID-19.Conclusions The mechanisms of LHQW capsule treating COVID-19 may involve in inhibiting inflammatory response, cytokine storm and virus infection, and regulating immune reactions, apoptosis and endothelial barrier.

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Quercetin Inhibits the Production of IL-1β-Induced Inflammatory Cytokines and Chemokines in ARPE-19 Cells via the MAPK and NF-κB Signaling Pathways

Cited by 173 publications

References 92 publications

Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells

Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells

The Role of Inflammation in Age-Related Macular Degeneration

Exploring the Mechanisms of Lian Hua Qing Wen Capsule against COVID-19 by Network Pharmacology and Molecular Docking Approach

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