scholarly journals Inhalation of Essential Oil from Mentha piperita Ameliorates PM10-Exposed Asthma by Targeting IL-6/JAK2/STAT3 Pathway Based on a Network Pharmacological Analysis

2020 ◽  
Vol 14 (1) ◽  
pp. 2
Author(s):  
Mi Hye Kim ◽  
Sang Jun Park ◽  
Woong Mo Yang
Keyword(s):  
Essential Oil ◽  
Signaling Pathway ◽  
Cell Activation ◽  
A549 Cells ◽  
Interaction Network ◽  
Mentha Piperita ◽  
Receptor Interaction ◽  
Pharmacological Analysis ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Fine particulate matter (PM) exposure exhibits a crucial risk factor to exacerbate airway epithelial remodeling, fibrosis, and pulmonary destruction in asthma. Based on the use of essential oils from aromatic plants on pain relief and anti-inflammatory properties, we investigated the inhibitory effects of essential oil derived from the Mentha species (MEO) against asthma exposed to PM10. The MEO (0.1 v/v %) was aerosolized by a nebulizer to ovalbumin and PM10-induced asthmatic mice. Histological changes were confirmed in the lung tissues. To define the mode of action of the MEO on asthma, a protein–protein interaction network was constructed using menthol and menthone as the major components of the MEO. Cytokine expression and the JAK2/STAT3 signaling pathway were analyzed in lung epithelial A549 cells co-treated with MEO and PM10. Inhalation of MEO by nebulization inhibited respiratory epithelium hyperplasia, collagen deposition, and goblet cell activation in asthmatic mice. Through a network pharmacological analysis, cytokine–cytokine receptor interaction and JAK/STAT was expected to be underlying mechanisms of MEO on asthma. Treatment with MEO significantly reduced the IL-6 levels with a decrease in pro-inflammatory and T helper 2-specific cytokines. PM10-induced phosphorylation of JAK2 and STAT3 was significantly decreased by MEO. Collectively, MEO may have an inhibitory effect on asthma under the condition of PM10 exposure through the IL-6/JAK2/STAT3 signaling pathway.

Mechanism of interaction between TM4SF1 and jak2-stat3 signaling pathway in lung cancer cells and expression analysis in non-small cell lung cancer

2020 ◽  
Author(s):  
Yumeng Niu ◽  
Hailong Deng ◽  
Lipeng Li ◽  
Weikang Chen ◽  
Yuxuan Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
A549 Cells ◽  
Normal Lung ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Stat3 Signaling ◽  
Skin Cancers ◽  
Stat3 Signaling Pathway ◽  
Cancer Tissues

Abstract Background According to the latest data released in 2018, it is estimated that there will be 18.1 million new cancer cases worldwide (excluding 1.7 million non-melanoma skin cancers) and 9.6 million cancer deaths (excluding 950 non-melanoma skin cancers) Million cases). Among them, the incidence of lung cancer (11.6% of the total number of cases) and mortality (18.4% of the total number of cancer deaths, which are expected to cause 1.8 million deaths) are the first. In recent years, studies have found TM4SF1 play an important role in the development process of many tumors.Methods Sixty-one patients with NSCLC who underwent surgical resection of cancer tissues, para-carcinoma tissues, and 10 normal lung tissues removed from benign lung disease (Jun/2018-Dec/2018) were collected. Real-time immunofluorescence quantitative PCR (qRT-PCR) and Western blot were used to detect the expression of TM4SF1 in NSCLC tissues (CT), para-carcinoma tissue (PCT), and normal lung tissues(NLT). TM4SF1 gene was overexpressed in lung cancer A549 cells using lentiviral transfection technology, qRT-PCR and Western blot were used to detect whether TM4SF1 gene was successfully expressed in lung cancer A549 cells, and Transwell was used to detect the effect of TM4SF1 overexpression on A549 migration. JAK2-STAT3 signal pathway interference reagent AG490 was used to analyze the expression levels of Stat3 and downstream Sox2 genes in the overexpression group, blank group, negative control group and their corresponding treatment groups TM4SF1, JAK2-STAT3 signal pathway using real-time qRT-PCR. Analyze the relevance of these three indicators at the same time.Results The expression levels of TM4SF1 mRNA and protein in cancer tissues were significantly higher than those in adjacent cancer tissues (P<0.05) and normal lung tissue specimens (P <0.05). The expression of TM4SF1 was not significantly associated with the age and sex of patients, but was associated with tumor size, degree of differentiation, lymph node metastasis, and clinical stage were related (P<0.05). TM4SF1 was successfully overexpressed in A549 cells. After overexpressing TM4SF1, the ability to migrate of A549 cells was significantly enhanced, and the expression levels of Stat3 and downstream Sox2 in the JAK2-STAT3 signaling pathway were up-regulated. The expression of TM4SF1, Stat3 and Sox2 at the mRNA level showed a positive correlation trend (P<0.01).Conclusion TM4SF1 is highly expressed in NSCLC, and its expression level is closely related to many clinical staging indicators. Overexpression of this gene can promote the migration of A549 cells and up-regulate the expression levels of Stat3 and downstream Sox2 in the JAK2-STAT3 signaling pathway. The expressions of TM4SF1, Stat3 and Sox2 were positively correlated in A549 cells. TM4SF1 may promote the occurrence, development and distant metastasis of NSCLC through this pathway. TM4SF1 may become a potential therapeutic target for NSCLC.

scholarly journals (–)-Catechin-7-O-β-d-Apiofuranoside Inhibits Hepatic Stellate Cell Activation by Suppressing the STAT3 Signaling Pathway

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 30 ◽  
Author(s):  
Yong Joo Park ◽  
Dong Min Kim ◽  
Mi Ho Jeong ◽  
Jae Sik Yu ◽  
Hae Min So ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cell ◽  
Cell Activation ◽  
Stellate Cell ◽  
Protective Effects ◽  
Inhibitory Effects ◽  
Etoh Extract ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Hepatic fibrosis is characterized by the abnormal deposition of extracellular matrix (ECM) proteins. During hepatic fibrogenesis, hepatic stellate cell (HSC) activation followed by chronic injuries is considered a key event in fibrogenesis, and activated HSCs are known to comprise approximately 90% of ECM-producing myofibroblasts. Here, we demonstrated that (–)-catechin-7-O-β-d-apiofuranoside (C7A) significantly inhibited HSC activation via blocking the signal transducer and activator of transcription 3 (STAT3) signaling pathway. This is the first study to show the hepatic protective effects of C7A with possible mechanisms in vitro and in vivo. In our bioactivity screening, we figured out that the EtOH extract of Ulmus davidiana var. japonica root barks, which have been used as a Korean traditional medicine, inhibited collagen synthesis in HSCs. Four catechins isolated from the EtOAc fraction of the EtOH extract were compared with each other in terms of reduction in collagen, which is considered as a marker of hepatic protective effects, and C7A showed the strongest inhibitory effects on HSC activation in protein and qPCR analyses. As a possible mechanism, we investigated the effects of C7A on the STAT3 signaling pathway, which is known to activate HSCs. We found that C7A inhibited phosphorylation of STAT3 and translocation of STAT3 to nucleus. C7A also inhibited expressions of MMP-2 and MMP-9, which are downstream genes of STAT3 signaling. Anti-fibrotic effects of C7A were evaluated in a thioacetamide (TAA)-induced liver fibrosis model, which indicated that C7A significantly inhibited ECM deposition through inhibiting STAT3 signaling. C7A decreased serum levels of aspartate amino transferase and alanine transaminase, which were markedly increased by TAA injection. Moreover, ECM-associated proteins and mRNA expression were strongly suppressed by C7A. Our study provides the experimental evidence that C7A has inhibitory effects on HSC activation after live injury and has preventive and therapeutic potentials for the management of hepatic fibrosis.

Lipopolysaccharide induces epithelial–mesenchymal transition of alveolar epithelial cells cocultured with macrophages possibly via the JAK2/STAT3 signaling pathway

2019 ◽  
Vol 39 (2) ◽  
pp. 224-234 ◽  
Author(s):  
Y Qin ◽  
P Zhao ◽  
Y Chen ◽  
X Liu ◽  
H Dong ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Inflammatory Markers ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Alveolar Epithelial Cells ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

Epithelial–mesenchymal transition (EMT) plays a key role in the process of pulmonary fibrosis (PF). Increasing evidences have shown that exaggerated EMT in recurrent pulmonary injury mediates the early pathogenesis of PF. This study aimed to evaluate EMT of human alveolar epithelial cells (A549) when cocultured with human macrophages Tohoku hospital pediatrics-1 (THP-1) induced by lipopolysaccharide (LPS) and investigate the role of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Firstly, we detected the inflammatory and EMT biomarkers in A549 cells monoculture and A549/THP-1 cells coculture in the presence or absence of LPS. Then, the activation of JAK2/STAT3 signaling pathway was determined in coculture. Interestingly, inflammatory markers, such as interleukin (IL)-6, matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)- β, and collagen type 1 (COL-1), were enhanced in LPS treated coculture. Besides, the expression of E-cadherin decreased but α-smooth muscle actin expression increased, indicating the presence of EMT in A549 cells when cocultured with THP-1 macrophages. However, these phenotypes could not be observed in LPS-treated A549 cells monoculture. Meanwhile, JAK2/STAT3 signaling pathway was activated, and the STAT3 DNA-binding and inflammatory markers were inhibited by Stattic. Together, these findings demonstrate the key role of JAK2/STAT3 signaling pathway in LPS promoted EMT of A549 in the presence of THP-1 macrophages as an in vitro PF model.

scholarly journals Activation of the STAT3 Signaling Pathway by the RNA-Dependent RNA Polymerase Protein of Arenavirus

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 976
Author(s):  
Qingxing Wang ◽  
Qilin Xin ◽  
Weijuan Shang ◽  
Weiwei Wan ◽  
Gengfu Xiao ◽  
...  
Keyword(s):  
Rna Polymerase ◽  
Signaling Pathway ◽  
Cell Biology ◽  
A549 Cells ◽  
Hemorrhagic Fever ◽  
Lymphocytic Choriomeningitis ◽  
Rna Dependent Rna Polymerase ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Transcription 3

Arenaviruses cause chronic and asymptomatic infections in their natural host, rodents, and several arenaviruses cause severe hemorrhagic fever that has a high mortality in infected humans, seriously threatening public health. There are currently no FDA-licensed drugs available against arenaviruses; therefore, it is important to develop novel antiviral strategies to combat them, which would be facilitated by a detailed understanding of the interactions between the viruses and their hosts. To this end, we performed a transcriptomic analysis on cells infected with arenavirus lymphocytic choriomeningitis virus (LCMV), a neglected human pathogen with clinical significance, and found that the signal transducer and activator of transcription 3 (STAT3) signaling pathway was activated. A further investigation indicated that STAT3 could be activated by the RNA-dependent RNA polymerase L protein (Lp) of LCMV. Our functional analysis found that STAT3 cannot affect LCMV multiplication in A549 cells. We also found that STAT3 was activated by the Lp of Mopeia virus and Junin virus, suggesting that this activation may be conserved across certain arenaviruses. Our study explored the interactions between arenaviruses and STAT3, which may help us to better understand the molecular and cell biology of arenaviruses.

Cucurbitacin I induces pro‐death autophagy in A549 cells via the ERK‐mTOR‐STAT3 signaling pathway

2018 ◽  
Vol 119 (7) ◽  
pp. 6104-6112 ◽  
Author(s):  
Yinyun Ni ◽  
Sisi Wu ◽  
Xiangxiu Wang ◽  
Guonian Zhu ◽  
Xuemei Chen ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
A549 Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway

scholarly journals Sphingosine-1-Phosphate Enhances Satellite Cell Activation in Dystrophic Muscles through a S1PR2/STAT3 Signaling Pathway

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37218 ◽  
Author(s):  
Kenneth C. Loh ◽  
Weng-In Leong ◽  
Morgan E. Carlson ◽  
Babak Oskouian ◽  
Ashok Kumar ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Satellite Cell ◽  
Cell Activation ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Sphingosine 1 Phosphate ◽  
Satellite Cell Activation

Aβ-induced microglial cell activation is inhibited by baicalin through the JAK2/STAT3 signaling pathway

2013 ◽  
Vol 124 (8) ◽  
pp. 609-620 ◽  
Author(s):  
Jiaxiang Xiong ◽  
Changzheng Wang ◽  
Hongyan Chen ◽  
Yazhuo Hu ◽  
Lei Tian ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cell Activation ◽  
Microglial Cell ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway
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