scholarly journals Apigenin alleviates TGF-β1-induced nasal mucosa remodeling by inhibiting MAPK / NF-kB signaling pathways in chronic rhinosinusitis

PLoS ONE ◽  
2018 ◽  
Vol 13 (8) ◽  
pp. e0201595 ◽  
Author(s):  
Hyun-Woo Yang ◽  
Hwee-Jin Kim ◽  
Joo-Hoo Park ◽  
Jae-Min Shin ◽  
Heung-Man Lee
Keyword(s):  
Signaling Pathways ◽  
Chronic Rhinosinusitis ◽  
Nasal Mucosa ◽  
Tgf Β1

scholarly journals Pengaruh Cuci Hidung dengan NaCl 0,9% Terhadap Ekspresi Gen IL-1Beta dan TNF-Alpha Mukosa Hidung Penderita Rinosinusitis Kronis di RSUP Dr M Djamil Padang

2019 ◽  
Vol 1 (2) ◽  
pp. 17-27
Author(s):  
Seres Triola
Keyword(s):  
Chronic Rhinosinusitis ◽  
Nasal Mucosa ◽  
Paranasal Sinuses ◽  
Nasal Wash ◽  
Postnasal Drip ◽  
Tnf Α ◽  
Before And After ◽  
Post Test ◽  
Absolute Expression ◽  
Tgf Β1

Chronic rhinosinusitis is an inflammatory disease of the nasal mucosa and paranasal sinuses which produces several proinflammatory cytokines including; IFN-γ, TGF-β1, IL-1β, IL-3, IL-6, IL-8, TNF-α, IL-5. The use of NaCl  0.9% nasal  wash in  chronic  rhinosinusitis  could reduce  mucin  secretion,  decrease  the  production  of postnasal  drip,  accelerate  mucosal  repair  and  reduce  the  symptoms  of  nasal  obstruction.  From  above, researchers want to know the effect of NaCl 0.9% nasal wash of the levels of cytokines IL-1β and TNF-α in the mucosa  of  the  nose  and  paranasal  sinuses  in  patients  with  chronic  rhinosinusitis.  This  research  is  an experimental study with the technique of pre and post test design to determine the effect of NaCl 0.9% nasal wash of the gene expression of IL-1β and TNF-α of nasal mucosa of patients with chronic rhinosinusitis. The amount  of IL-1β gene copynumber before and  after nasal  wash is  obtained 8.07 ± 0.95  and 8,20 ± 0.93 (p >0.05). The amount of TNF-α gene copynumber before and after nasal wash was 8,83 ±3,83 and 6,72 ±2,55 (p >0.05). IL-1β gene ratio starting and ending intervention in two groups was 52,51 ± 1.21 and 61,99 ± 1.13. TNF-α gene ratio starting and ending intervention in two groups was 9,63 ±2.21 and 334,4 ±1.31. In this study there was no significant reduction in the absolute expression (log copynumber) gene IL-1β and TNF-α of nasal mucosa after being given medical treatment with NaCl 0,9% nasal wash.

scholarly journals Urolithin A attenuates renal fibrosis by inhibiting TGF-β1/Smad and MAPK signaling pathways

2021 ◽  
Vol 83 ◽  
pp. 104547
Author(s):  
Zhenzhen Cheng ◽  
Jingjing Tu ◽  
Hongpan Zhang ◽  
Yi zhang ◽  
Benhong Zhou
Keyword(s):  
Signaling Pathways ◽  
Renal Fibrosis ◽  
Mapk Signaling ◽  
Urolithin A ◽  
Mapk Signaling Pathways ◽  
Tgf Β1

scholarly journals CD133, a Progenitor Cell Marker, is Reduced in Nasal Polyposis and Showed Significant Correlations with TGF-β1 and IL-8

2021 ◽  
Author(s):  
Wagner Vargas Souza Lino ◽  
André Luis Lacerda Bachi ◽  
José Arruda Mendes Neto ◽  
Gabriel Caetani ◽  
Jônatas Bussador do Amaral ◽  
...  
Keyword(s):  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Nasal Polyposis ◽  
Transforming Growth Factor ◽  
Middle Turbinate ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Histologic Analysis ◽  
Aspirin Intolerance ◽  
Tgf Β1

Abstract Introduction Combination of chronic inflammation and an altered tissue remodeling process are involved in the development of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP). Studies demonstrated that mesenchymal stem cells expressing the progenitor gene CD133 were involved in a significant reduction of the chronic inflammatory process in the polypoid tissue. Objective To evaluate the levels of CD133 (Prominin-1) in nasal polypoid tissue and its correlation with interleukin-8 (IL-8) and transforming growth factor β1 (TGF-β1). Methods A total of 74 subjects were divided in the following groups: control group (n = 35); chronic rhinosinusitis with nasal polyps nonpresenting comorbid asthma and aspirin intolerance (CRSwNPnonAI) group (n = 27); and chronic rhinosinusitis with nasal polyps presenting comorbid asthma and aspirin intolerance (CRSwNPAI) group (n = 12). Histologic analysis and also evaluation of the concentration of CD133, IL-8, and TGF-β1 by enzyme-linked immunosorbent assay (ELISA) kits were performed in nasal tissue obtained from nasal polypectomy or from middle turbinate tissue. Results Higher eosinophilic infiltration was found in both CRSwNP groups by histologic analysis. Lower levels of TGF-β1 and IL-8 were observed in both CRSwNP groups when compared with the control group, whereas the CD133 levels were significantly reduced only in the CRSwNPnonAI group compared with the control group. Conclusion It was demonstrated that the nasal mucosa presenting polyposis showed a significant reduction of CD133 levels, and also that this reduction was significantly correlated with the reduction of TGF-β1 levels, but not with IL-8 levels. Therefore, these findings may be involved in the altered inflammatory and remodeling processes observed in the nasal polyposis.

scholarly journals TGF-β1 targets Smad, p38 MAPK, and PI3K/Akt signaling pathways to induce PFKFB3 gene expression and glycolysis in glioblastoma cells

FEBS Journal ◽  
2017 ◽  
Vol 284 (20) ◽  
pp. 3437-3454 ◽  
Author(s):  
Ana Rodríguez-García ◽  
Paula Samsó ◽  
Pere Fontova ◽  
Helga Simon-Molas ◽  
Anna Manzano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Akt Signaling ◽  
Glioblastoma Cells ◽  
Tgf Β1

scholarly journals LTD4 and TGF-β1 Induce the Expression of Metalloproteinase-1 in Chronic Rhinosinusitis via a Cysteinyl Leukotriene Receptor 1-Related Mechanism

Sinusitis ◽  
2016 ◽  
Vol 1 (1) ◽  
pp. 65-75
Author(s):  
Rogerio Pezato ◽  
Cindy Claeys ◽  
Gabriele Holtappels ◽  
Claus Bachert ◽  
Claudina Pérez-Novo
Keyword(s):  
Chronic Rhinosinusitis ◽  
Cysteinyl Leukotriene ◽  
Leukotriene Receptor ◽  
Cysteinyl Leukotriene Receptor ◽  
Tgf Β1

scholarly journals Potential Mechanism Prediction of Herbal Medicine for Pulmonary Fibrosis Associated with SARS-CoV-2 Infection Based on Network Analysis and Molecular Docking

2021 ◽  
Vol 12 ◽  
Author(s):  
De Jin ◽  
Xuedong An ◽  
Yuqing Zhang ◽  
Shenghui Zhao ◽  
Liyun Duan ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Pulmonary Fibrosis ◽  
Signaling Pathways ◽  
Topological Analysis ◽  
Recovery Period ◽  
Treatment Protocol ◽  
Docking Simulation ◽  
Mapk Signaling ◽  
Tnf Α ◽  
Tgf Β1

Background: Coronavirus Disease 2019 (COVID-19) is still a relevant global problem. Although some patients have recovered from COVID-19, the sequalae to the SARS-CoV-2 infection may include pulmonary fibrosis, which may contribute to considerable economic burden and health-care challenges. Convalescent Chinese Prescription (CCP) has been widely used during the COVID-19 recovery period for patients who were at high risk of pulmonary fibrosis and is recommended by the Diagnosis and Treatment Protocol for COVID-19 (Trial Version sixth, seventh). However, its underlying mechanism is still unclear.Methods: In this study, an integrated pharmacology approach was implemented, which involved evaluation of absorption, distribution, metabolism and excretion of CCP, data mining of the disease targets, protein-protein interaction (PPI) network construction, and analysis, enrichment analysis, and molecular docking simulation, to predict the bioactive components, potential targets, and molecular mechanism of CCP for pulmonary fibrosis associated with SARS-CoV-2 infection.Results: The active compound of CCP and the candidate targets, including pulmonary fibrosis targets, were obtained through database mining. The Drug-Disease network was constructed. Sixty-five key targets were identified by topological analysis. The findings of Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation suggested that the VEGF, Toll-like 4 receptor, MAPK signaling pathway, and TGF-β1 signaling pathways may be involved in pulmonary fibrosis. In the molecular docking analyses, VEGF, TNF-α, IL-6, MMP9 exhibited good binding activity. Findings from our study indicated that CCP could inhibit the expression of VEGF, TNF-α, IL-6, MMP9, TGF-β1 via the VEGF, Toll-like 4 receptor, MAPK, and TGF-β1 signaling pathways.Conclusion: Potential mechanisms involved in CCP treatment for COVID-19 pulmonary fibrosis associated with SARS-CoV-2 infection involves multiple components and multiple target points as well as multiple pathways. These findings may offer a profile for further investigations of the anti-fibrotic mechanism of CCP.

Sign in / Sign up

Export Citation Format

Share Document