inflammation/никотин

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Nicotine induces pro-inflammatory response in aortic vascular smooth muscle cells through a NFκB/osteopontin amplification loop-dependent pathway.

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Nicotine has anti- and pro-inflammatory properties in various cells. Its role in aortic vascular smooth muscle cells (VSMC) was explored. Human aortic VSMC were cultured. After nicotine (1.0 μM) and/or pyrrolidinedithiocarbamic acid (PDTC, 50 μM) treatment, the activation of nuclear factor κB (NFκB)

Nicotine enhances ethanol-induced fat accumulation and collagen deposition but not inflammation in mouse liver.

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BACKGROUND Alcohol and tobacco are frequently co-abused. Tobacco smoke increases alcoholic steatosis in apoE(-/-) mice. Tobacco smoke contains more than 4000 chemicals, but it is unknown which compounds in tobacco smoke play a major role in increasing alcoholic steatosis. METHODS C57BL/J6 mice were

Nicotine Modulates the Release of Inflammatory Cytokines and Expression of TLR2, TLR4 of Cord Blood Mononuclear Cells.

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The underlying mechanisms of how nicotine affects cord umbilical cells remain largely elusive. Nicotine rapidly crosses the blood-brain barrier (10 to 20 s) and binds to nicotinic acetylcholine receptors (nAChRs). Nicotine considered as a major compound found in cigarette smoke and the mechanism of

Anti-interleukin-17 antibodies attenuate airway inflammation in tobacco-smoke-exposed mice.

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BACKGROUND Our previous study showed that the interleukin-17 (IL-17) concentration in lung tissue and in bronchoalveolar lavage fluid (BALF) of rats with tobacco-smoke-induced chronic obstructive pulmonary disease (COPD) was higher than that of control group. However, whether IL-17 inhibitor could

Influence of ferulic acid on nicotine-induced lipid peroxidation, DNA damage and inflammation in experimental rats as compared to N-acetylcysteine.

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We examined the effect of ferulic acid (FA), a naturally occurring phenolic compound on lipid peroxidation and endogenous antioxidant status, DNA damage and inflammation in nicotine-administered Wistar rats. The effect of FA against nicotine toxicity was compared with N-acetylcysteine (NAC), a

The Intersection of Sex Differences, Tobacco Use, and Inflammation: Implications for Psychiatric Disorders.

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OBJECTIVE Tobacco use, sex differences, and psychiatric disorders are associated with altered immune function. There are also sex differences in tobacco use and psychiatric disorders. This review summarizes findings from the small, but growing literature examining sex differences in the effects of

Chronic low-grade peripheral inflammation is associated with severe nicotine dependence in schizophrenia: results from the national multicentric FACE-SZ cohort.

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Chronic peripheral inflammation (CPI) has been associated with cognitive impairment in schizophrenia (SZ). However, its sources remain unclear, more specifically it is not known whether tobacco smoking is a source of inflammation or not in SZ subjects. Moreover, nicotine (NIC), the major

Toll-like receptor-9 agonist inhibits airway inflammation, remodeling and hyperreactivity in mice exposed to chronic environmental tobacco smoke and allergen.

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BACKGROUND As passive environmental tobacco smoke (ETS) exposure in nonsmokers can increase both asthma symptoms and the frequency of asthma exacerbations, we utilized a mouse model, in which ovalbumin (OVA) + ETS induce significantly increased levels of eosinophilic airway inflammation and

Selenium nanoparticles with low-level ionizing radiation exposure ameliorate nicotine-induced inflammatory impairment in rat kidney.

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Occupational exposure to low-level ionizing radiation (<1 Gy) was shown to enhance cell protection via attenuating an established inflammatory process. Nicotine, a major toxic component of cigarette smoke, is responsible for smoking-mediated renal dysfunction. The present study was therefore aimed

Cannabinoid CB2 Receptor Mediates Nicotine-Induced Anti-Inflammation in N9 Microglial Cells Exposed to β Amyloid via Protein Kinase C.

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BACKGROUND Reducing β amyloid- (Aβ-) induced microglial activation is considered to be effective in treating Alzheimer's disease (AD). Nicotine attenuates Aβ-induced microglial activation; the mechanism, however, is still elusive. Microglia could be activated into classic activated state (M1 state)

Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect.

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Cholinergic anti-inflammatory pathway has therapeutic effect on inflammation-associated diseases. However, the exact mechanism of nicotine-mediated anti-inflammatory effect is still unclear. TIPE2, a new member of tumor necrosis factor-α-induced protein-8 family, is a negative regulator of immune

4-O-methylhonokiol inhibits serious embryo anomalies caused by nicotine via modulations of oxidative stress, apoptosis, and inflammation.

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BACKGROUND Since the increasing smoking rate among women has resulted in higher rates of embryonic malformations, it is important to search for an efficient and inexpensive agent that can help reduce the rate of serious fetal anomalies caused by maternal cigarette smoking. In this study, the

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis.

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Ulcerative colitis (UC) is characterized by impairment of the epithelial barrier and the formation of ulcer-type lesions, which result in local leaks and generalized alterations of mucosal tight junctions. Ultimately, this results in increased basal permeability. Although disruption of the

IQOS - a heat-not-burn (HnB) tobacco product - chemical composition and possible impact on oxidative stress and inflammatory response. A systematic review.

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Objectives: This work attempts to summarize current knowledge about IQOS, the heat-not-burn tobacco products, their chemical composition and possible impact on oxidative stress and inflammatory response. Materials and Methods: The literature search was performed between January and

The role of the CCR1 receptor in the inflammatory response to tobacco smoke in a mouse model.

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OBJECTIVE The aim was to create pathological changes in mice relevant to human smoke exposure that can be used to further understand the mechanisms and pathology of smoke-induced inflammatory disease. METHODS Mice were exposed to tobacco smoke or lipopolysaccharide (LPS) to generate an inflammatory

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