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Drug: Nicotine

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Total 48 results found since Jan 2013.

SOCS3 participates in cholinergic pathway regulation of synovitis in rheumatoid arthritis.
This study investigated the effect of SOCS on cholinergic pathway regulation of synovitis in the fibroblast-like synoviocytes (FLSs) of RA and CIA mice. The effects of nicotine on SOCS1 and SOCS3 protein expression in FLSs were assayed by western blotting before and after transfection with a small interfering RNA oligonucleotide (SOCS3-siRNA or control-siRNA). Interleukin-6 was measured by enzyme-linked immunosorbent assay of SOCS3-siRNA and control-siRNA transfected FLS culture supernatants. Histopathological evaluation and immunohistochemical staining of SOCS3 were performed in joint tissue sections of control, CIA model...
Source: Connective Tissue Research - September 17, 2017 Category: Research Tags: Connect Tissue Res Source Type: research

Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts.
Abstract Cigarette smoke is the major cause of chronic obstructive pulmonary disease (COPD), yet pathogenic mechanisms are not fully understood. Vascular endothelial growth factor (VEGF) is one of the major regulators of endothelial cell survival and is believed to play a role in the pathogenesis of COPD. Fibroblasts are a significant source of VEGF in the lungs; however the effect of cigarette smoke exposure on VEGF release by fibroblasts is not fully understood. We hypothesized that cigarette smoke-induced disturbed VEGF release by human lung fibroblasts is a potential pathogenic mechanism that could contribute ...
Source: Toxicology Letters - April 22, 2013 Category: Toxicology Authors: Farid M, Kanaji N, Nakanishi M, Gunji Y, Michalski J, Iwasawa S, Ikari J, Wang X, Basma H, Nelson AJ, Liu X, Rennard SI Tags: Toxicol Lett Source Type: research

Nicotine Induced Epithelial-Mesenchymal Transition via Wnt/β-catenin Signaling in Human Airway Epithelial Cells.
Conclusion: These results suggest that HBECs are able to undergo EMT in vitro upon nicotine stimulation via the Wnt3a/β-catenin signaling pathway. PMID: 23204070 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - November 30, 2012 Category: Cytology Authors: Zou W, Zou Y, Zhao Z, Li B, Ran P Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Nicotine-induced epithelial-mesenchymal transition via Wnt/{beta}-catenin signaling in human airway epithelial cells
Epithelial-mesenchymal transition (EMT) has been proposed to be a mechanism in airway remodeling, which is a characteristic of chronic obstructive pulmonary disease (COPD). Studies have shown that cigarette smoke and nicotine are factors that induce Wnt/β-catenin activation, which is a pathway that has also been implicated in EMT. The main aim of this study was to test whether human bronchial epithelial cells are able to undergo EMT in vitro following nicotine stimulation via the Wnt3a/β-catenin signaling pathway. We show that nicotine activates the Wnt3a signal pathway, which leads to the translocation of β...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2013 Category: Respiratory Medicine Authors: Zou, W., Zou, Y., Zhao, Z., Li, B., Ran, P. Tags: CALL FOR PAPERS Source Type: research

Nicotine potentiates oxLDL-induced proatherogenic effects via stimulating and upregulating macrophage CD36 signaling.
Abstract Cigarette smoking is a major risk factor for atherosclerosis and cardiovascular disease. CD36 mediates oxLDL uptake and contributes to macrophage foam cell formation. We investigated a role for the CD36 pathway in nicotine-induced activation of macrophages and foam cell formation in vitro and in vivo. Nicotine in the same plasma concentration range found in smokers increased the CD36(+)/CD14(+) cell population in human peripheral blood mononuclear cells, increased CD36 expression of human THP1 macrophages and increased macrophage production of reactive oxygen species, PKCδ phosphorylation and PPARγ expr...
Source: American Journal of Physiology. Heart and Circulatory Physiology - June 7, 2013 Category: Physiology Authors: Zhou MS, Chadipiralla K, Mendez AJ, Jaimes EA, Silverstein RL, Webster KA, Raij L Tags: Am J Physiol Heart Circ Physiol Source Type: research

Neutral endopeptidase regulates neurogenic inflammatory responses induced by stimulation of human oral keratinocytes with bacterial lipopolysaccharide and nicotine
In conclusion, the present study demonstrated that NEP down‐regulated the levels of SP and IL‐1β produced from human oral keratinocytes, although ECE‐1 may be partly related to the down‐regulation.
Source: European Journal of Oral Sciences - July 17, 2013 Category: Dentistry Authors: Motoki Nakata, Shuji Awano, Naomasa Kinoshita, Akihiro Yoshida, Toshihiro Ansai Tags: Original Article Source Type: research

Nicotine-mediated invasion and migration of non-small cell lung carcinoma cells by modulating STMN3 and GSPT1 genes in an ID1-dependent manner
Conclusions: Collectively, our data suggests that nicotine and EGF induce genes such as STMN3 and GSPT1 to promote the proliferation, invasion and migration of NSCLC, thus enhancing their tumorigenic properties. These studies thus reveal a central role for ID1 and its downstream targets in facilitating lung cancer progression.
Source: Molecular Cancer - July 16, 2014 Category: Cancer & Oncology Authors: Sajitha NairNamrata Bora-SinghalDeepak PerumalSrikumar Chellappan Source Type: research

Role of resistin in the inflammatory response induced by nicotine plus lipopolysaccharide in human periodontal ligament cells in vitro
ConclusionThis is the first study to show that the inhibition of resistin, by either a pharmacological or a genetic silencing approach, has anti‐inflammatory effects. These effects include decreased levels of inflammatory cytokines and the prevention of ECM breakdown in a nicotine plus LPS‐stimulated PDLC model.
Source: Journal of Periodontal Research - November 13, 2014 Category: Dentistry Authors: S.‐K. Kang, Y.‐D. Park, S.‐I. Kang, D.‐K. Kim, K.‐L. Kang, S.‐Y. Lee, H.‐J. Lee, E.‐C. Kim Tags: Original Article Source Type: research

Regulation of Cigarette Smoke Induction of IL‐8 in Macrophages by AMP‐activated Protein Kinase Signaling
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - December 11, 2014 Category: Cytology Authors: Hsin‐Kuo Ko, Hung‐Fu Lee, An‐Hsuan Lin, Meng‐Han Liu, Ching‐I Liu, Tzong‐Shyuan Lee, Yu Ru Kou Tags: Original Research Article Source Type: research

HIF‐2 inhibition supresses inflammatory responses and osteoclastic differentiation in human periodontal ligament cells
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Biochemistry - January 7, 2015 Category: Biochemistry Authors: Won‐Jung Bae, Mee‐Ran Shin, Soo‐Kyung Kang, Zhang Jun, Jun‐Yeol Kim, Sang‐Cheon Lee, Eun‐Cheol Kim Tags: Article Source Type: research

Activation of Nicotinic Receptors Inhibits TNF-α-Induced Production of Pro-inflammatory Mediators Through the JAK2/STAT3 Signaling Pathway in Fibroblast-Like Synoviocytes
In conclusion, nicotine has an anti-inflammatory effect on RA by downregulating production of IL-6 and MCP-1 in FLSs, and this is mediated through activation of the JAK2–STAT3 signal pathway.
Source: Inflammation - January 23, 2015 Category: Allergy & Immunology Source Type: research

α5-nAChR modulates nicotine-induced cell migration and invasion in A549 lung cancer cells.
Abstract Cigarette smoking is the most important risk factor in the development of human lung cancer. Nicotine, the major component in tobacco, not only contributes to carcinogenesis but also promotes tumor metastasis. By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and migration of non-small cell lung cancer. Recently studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. Nevertheless, it is unclear whether nicotine promotes the migration and invasion through activation of α5-nAChR in lung cancer. In the present study...
Source: Experimental and Toxicologic Pathology - July 20, 2015 Category: Pathology Authors: Sun H, Ma X Tags: Exp Toxicol Pathol Source Type: research

Wnt/ β-catenin signaling plays an essential role in α7 nicotinic receptor-mediated neuroprotection of dopaminergic neurons in a mouse Parkinson's disease model.
The objective of the present study was to explore the potential functions of α7-nAChRs in PD pathology, and to determine whether these effects are exerted via Wnt/β-catenin signaling in a mouse PD model. In the in vivo study, α7-nAChR knockout (α7-KO) reversed the beneficial effects of nicotine on motor deficits, dopaminergic neuron loss, astrocyte and microglia activation, and reduced striatal dopamine release induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Injury to SH-SY5Y cells by 1-methyl-4-phenylpyridinium treatment was also ameliorated by nicotine, and this effect was abolished by methyllycaconitine (ML...
Source: Biochemical Pharmacology - May 24, 2017 Category: Drugs & Pharmacology Authors: Liu Y, Hao S, Yang B, Fan Y, Qin X, Chen Y, Hu J Tags: Biochem Pharmacol Source Type: research

Carbon monoxide-releasing molecule suppresses inflammatory and osteoclastogenic cytokines in nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via the heme oxygenase-1 pathway.
Abstract Smoking is identified as a risk factor for periodontitis. Carbon monoxide (CO)-releasing molecule-3 (CORM-3) is a compound that has demonstrated anti-inflammatory effects in vitro and in vivo studies. The present study aimed to investigate the effects of CORM-3 on the expression of inflammatory and osteoclastogenic cytokines in human periodontal ligament cells (PDLCs) stimulated by nicotine and lipopolysaccharide (LPS). The cells were pretreated with CORM-3 and then cultured in medium in the presence of nicotine and LPS. The mRNA and protein expression levels of prostaglandin E2 (PGE2), cyclooxygenas...
Source: International Journal of Molecular Medicine - September 8, 2017 Category: Molecular Biology Authors: Song L, Li J, Yuan X, Liu W, Chen Z, Guo D, Yang F, Guo Q, Song H Tags: Int J Mol Med Source Type: research

Sinomenine increases adenosine A < sub > 2A < /sub > receptor and inhibits NF- κB to inhibit arthritis in adjuvant-induced-arthritis rats and fibroblast-like synoviocytes through α7nAChR
J Leukoc Biol. 2021 Aug 23. doi: 10.1002/JLB.3MA0121-024RRRR. Online ahead of print.ABSTRACTSinomenine (SIN) is a clinical drug for treating rheumatoid arthritis (RA) in China. Our previous study found SIN inhibited inflammation via alpha7 nicotinic acetylcholine receptor (α7nAChR) in macrophages in vitro. Adenosine receptor A2A has anti-inflammatory and immunosuppressive function. However, the mechanisms of SIN acting on α7nAChR and the effect on adenosine A2A receptor (A2A R) in RA are not clear. In the present study, the effects of SIN on adjuvant-induced-arthritis (AIA) rats in vivo and on fibroblast-like synoviocyte...
Source: Journal of Leukocyte Biology - August 23, 2021 Category: Hematology Authors: Lang Yi Junyu Ke Jiayan Liu Huili Lai Yanjun Lv Chong Peng Yingkun Zhi Qun Du Liang Liu Peixun Wang Hua Zhou Yan Dong Source Type: research