Progressive Increase in Platelet Activation With Smoke Exposure: Human Subject and In-Vitro Studies

2007 ◽  
Author(s):  
Gaurav Girdhar ◽  
Sulan Xu ◽  
Jolyon Jesty ◽  
Danny Bluestein
Keyword(s):  
Cigarette Smoke ◽  
Platelet Activation ◽  
Human Subject ◽  
Prolonged Exposure ◽  
Human Subjects ◽  
Progressive Increase ◽  
In Vitro Studies ◽  
Protective Effects ◽  
Shs Exposure

Second hand cigarette smoke (SHS) is one of the major risk factors for cardiovascular disease (CVD) and has been shown to substantiate platelet activation and aggregation in several studies [1, 2]. Most of these studies, under chronic or acute exposure conditions or over prolonged exposure, do not represent the initiation of a disease state or hematological damage under normal levels of cigarette smoke. These above studies of platelet activation with SHS together with our previous in-vitro studies demonstrating cardio-protective effects of nicotine [3], have motivated the present investigation of physiological levels of SHS exposure on human subjects and within an in-vitro endothelial cell-platelet system, with cigarettes (or smoke extracts) of varying nicotine content to confirm analogous cardio-protective effects of nicotine.

In vitro studies of biological effects of cigarette smoke condensate

1985 ◽  
Vol 157 (2-3) ◽  
pp. 169-180 ◽  
Author(s):  
Margareta Curvall ◽  
Tommy Jansson ◽  
Bertil Pettersson ◽  
Annica Hedin ◽  
Curt R. Enzell
Keyword(s):  
Cigarette Smoke ◽  
Biological Effects ◽  
In Vitro Studies ◽  
Cigarette Smoke Condensate

Inhibition of oral peroxidase activity by cigarette smoke: in vivo and in vitro studies

2003 ◽  
Vol 34 (3) ◽  
pp. 377-384 ◽  
Author(s):  
Abraham Z Reznick ◽  
Ifat Klein ◽  
Jason P Eiserich ◽  
Carroll E Cross ◽  
Rafael M Nagler
Keyword(s):  
Cigarette Smoke ◽  
Peroxidase Activity ◽  
In Vitro Studies

Anthocyanins from red cabbage extract — evidence of protective effects on blood platelets

2012 ◽  
Vol 7 (4) ◽  
pp. 655-663 ◽  
Author(s):  
Joanna Saluk ◽  
Michał Bijak ◽  
Joanna Kołodziejczyk-Czepas ◽  
Małgorzata Posmyk ◽  
Krystyna Janas ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Platelet Activation ◽  
Blood Platelets ◽  
Protective Effects ◽  
Platelet Activity ◽  
Red Cabbage ◽  
Arachidonate Cascade ◽  
Wide Range ◽  
Antioxidative Effects

AbstractRed cabbage belongs to cruciferous vegetables recognized as a rich source of anthocyanins. Anthocyanins have a wide range of therapeutic advantages without adverse effects, including cardiovascular protective properties. For development of cardiovascular diseases, platelet activation is crucial; therefore compounds which inhibit platelet activation are sought after. The anti-platelet activity of anthocyanins has only been described and is still unclear. In our study, the extract of anthocyanins, obtained from fresh leaves of red cabbage, was used in vitro to examine their antioxidative effects on platelets under oxidative stress conditions which are responsible for hyperactivity of these cells. The antiplatelet and antioxidative activities were determined by platelet aggregation and specific markers of the arachidonate cascade with O2−· generation, and oxidative changes (carbonyl groups and 3-nitrotyrosine). Extracts (5–15 μM) protected platelet proteins and lipids against oxidative damage, and diminished platelet activation. Anthocyanins from red cabbage provided beneficial anti-platelet effects and might help prevent cardiovascular diseases.

In vitro studies of biological effects of cigarette smoke condensate

1986 ◽  
Vol 169 (3) ◽  
pp. 129-139 ◽  
Author(s):  
Tommy Jansson ◽  
Margareta Curvall ◽  
Annica Hedin ◽  
Curt R. Enzell
Keyword(s):  
Cigarette Smoke ◽  
Biological Effects ◽  
In Vitro Studies ◽  
Cigarette Smoke Condensate

scholarly journals CCN1 secretion and cleavage regulate the lung epithelial cell functions after cigarette smoke

2014 ◽  
Vol 307 (4) ◽  
pp. L326-L337 ◽  
Author(s):  
Hyung-Geun Moon ◽  
Sang-Heon Kim ◽  
Jinming Gao ◽  
Taihao Quan ◽  
Zhaoping Qin ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cigarette Smoke ◽  
Prolonged Exposure ◽  
Cell Damage ◽  
Lung Epithelial Cells ◽  
Tissue Loss ◽  
Cell Functions ◽  
Lung Epithelial

Despite extensive research, the pathogenesis of cigarette smoking (CS)-associated emphysema remains incompletely understood, thereby impeding development of novel therapeutics, diagnostics, and biomarkers. Here, we report a novel paradigm potentially involved in the development of epithelial death and tissue loss in CS-associated emphysema. After prolonged exposure of CS, CCN1 cleavage was detected both in vitro and in vivo. Full-length CCN1 (flCCN1) was secreted in an exosome-shuttled manner, and secreted plasmin converted flCCN1 to cleaved CCN1 (cCCN1) in extracellular matrix. Interestingly, exosome-shuttled flCCN1 facilitated the interleukin (IL)-8 and vascular endothelial growth factor (VEGF) release in response to cigarette smoke extract (CSE). Therefore, flCCN1 potentially promoted CS-induced inflammation via IL-8-mediated neutrophil recruitment and also maintained the lung homeostasis via VEGF secretion. Interestingly, cCCN1 abolished these functions. Furthermore, cCCN1 promoted protease and matrix metalloproteinase (MMP)-1 production after CSE. These effects were mainly mediated by the COOH-terminal fragments of CCN1 after cleavage. Both the decrease of VEGF and the elevation of MMPs favor the development of emphysema. cCCN1, therefore, likely contributes to the epithelial cell damage after CS. Additionally, CSE and cCCN1 both stimulated integrin-α7 expressions in lung epithelial cells. The integrin-α7 appeared to be the binding receptors of cCCN1 and, subsequently, mediated its cellular function by promoting MMP1. Consistent with our observation on the functional roles of cCCN1 in vitro, elevated cCCN1 level was found in the bronchoalveolar lavage fluid from mice with emphysematous changes after 6 mo CS exposure. Taken together, we hypothesize that cCCN1 promoted the epithelial cell death and tissue loss after prolonged CS exposure.

scholarly journals Beneficial Effects of Naringenin in Cigarette Smoke-Induced Damage to the Lung Based on Bioinformatic Prediction and In Vitro Analysis

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4704
Author(s):  
Pan Chen ◽  
Ziting Xiao ◽  
Hao Wu ◽  
Yonggang Wang ◽  
Weiyang Fan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Bioinformatic Analysis ◽  
Protective Effects ◽  
Nrf2 Pathway ◽  
Beneficial Effects ◽  
Aryl Hydrocarbon ◽  
Vitro Analysis ◽  
Lung Health

Naringenin is found mainly in citrus fruits, and is thought to be beneficial in the prevention and control of lung diseases. This study aims to investigate the mechanisms of naringenin against the damage in the lung caused by cigarette smoke. A system bioinformatic approach was proposed to predict the mechanisms of naringenin for protecting lung health. Then, we validated this prediction in BEAS-2B cells treated with cigarette smoke extract (CSE). System bioinformatic analysis indicated that naringenin exhibits protective effects on lung through the inhibition of inflammation and suppression of oxidative stress based on a multi-pathways network, mainly including oxidative stress pathway, Nrf2 pathway, Lung fibrosis pathway, IL-3 signaling pathway, and Aryl hydrocarbon receptor pathway. The in vitro results showed that naringenin significantly attenuated CSE-induced up-regulation of IL-8 and TNF-α. CSE stimulation increased the mRNA expressions of Nrf2, HO-1, and NQO1; the levels of total protein and nuclear protein of Nrf2; and the activity of SOD on days 2 and 4; but decreased these indexes on day 6. Naringenin can balance the antioxidant system by regulating Nrf2 and its downstream genes, preliminarily validating that Nrf2 pathway is involved in the protection offered by naringenin against cigarette smoke-induced damage to the lung. It suggests that dietary naringenin shows possible potential use in the management of lung health.

E-Selectin Expression on Endothelial Cells in the Presence of Platelets and Cigarette Smoke Extract

2008 ◽  
Author(s):  
Gaurav Girdhar ◽  
Sulan Xu ◽  
Jolyon Jesty ◽  
Danny Bluestein
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Platelet Activation ◽  
Cigarette Smoke Extract ◽  
Shear Stresses ◽  
Couette Viscometer ◽  
Activated Platelets ◽  
High Concentrations ◽  
Cv Disease

Cigarette smoking is a risk factor for development of cardiovascular (CV) disease [1], with increased platelet activation due to cigarette smoke involving a major part of this risk.[2] We have shown that this smoke-induced platelet activation is largely due to the non-nicotine smoke components and their effects can be effectively modulated in the presence of nicotine.[3] However, the effects of nicotine and non-nicotine cigarette smoke components need to be confirmed more physiologically in the presence of endothelial cells (ECs). Prior in-vitro studies have shown that high concentrations of cigarette smoke extract (CSE) increase adhesion molecule expression on ECs.[4] These studies however preclude the involvement of physiological shear stresses and are performed on ECs alone. To overcome these limitations and investigate ECs-platelets together in one system under shear stress, we use a hemodynamic shear device (HSD) that combines features of the cone and plate, and the annular Couette viscometer (to facilitate platelet sampling). We test the following hypotheses — (1) smoke-activated platelets and the nicotine-free extract would confer a synergistic E-selectin expression on ECs, and (2) in contrast to conventional cigarette extracts, nicotine-free smoke extracts would increase platelet activation more significantly, and that this effect may be independent of the presence of ECs.

Polyphenols: Anti-Platelet Nutraceutical?

2018 ◽  
Vol 24 (2) ◽  
pp. 146-157 ◽  
Author(s):  
Valeria Ludovici ◽  
Jens Barthelmes ◽  
Matthias P. Nagele ◽  
Andreas J. Flammer ◽  
Isabella Sudano
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Therapeutic Potential ◽  
Critical Role ◽  
Organ Damage ◽  
Low Grade ◽  
Protective Effects ◽  
Dietary Polyphenols

Background: Coronary artery disease (CAD) is a disease progressing over many years. Genetic factors, as well as the exposure to risk factors, are continuously leading to endothelial dysfunction, vascular alterations and, eventually, organ damage, major cardiovascular events and deaths. Oxidative stress, platelet hyperactivity and low-grade inflammation are important modulators in this context, contributing to plaque formation. Since platelet activation plays a critical role in the development and progression of atherothrombotic events, the inhibition of platelet hyperactivity may contribute to decreased atherothrombotic risk. The consumption of bioactive foods, and plant-derived polyphenols in particular, might impart anti-thrombotic and cardiovascular protective effects. Methods: Aim of this work is to focus on the potential of dietary derived polyphenols to reduce platelet hyperactivity or hypercoagulability in addition to discussing their possible complementary anti-platelet therapeutic potential. All the relevant publications on this topic were systematically reviewed. Results: Various studies demonstrated that polyphenol supplementation affects platelet aggregation and function in vitro and in vivo, mainly neutralizing free radicals, inhibiting platelet activation and related signal transduction pathways, blocking thromboxane A2 receptors and enhancing nitric oxide production. Experimental data concerning the effect of dietary polyphenols on platelet aggregation in vivo are poor, and results are often conflicting. Only flavanols clearly mirrored in vivo showed the efficacy in vitro in modulating platelet function. Conclusion: Dietary polyphenols, and above all flavanols contained in cocoa and berries, reduce platelet activation and aggregation via multiple pathways. However, more controlled interventional studies are required to establish which doses are required as well as what circulating concentrations are sufficient to induce functional antiplatelet effects.

Protective effects of isorhamnetin on pulmonary arterial hypertension: in vivo and in vitro studies

2020 ◽  
Vol 34 (10) ◽  
pp. 2730-2744
Author(s):  
Zhi Chang ◽  
Jia‐ling Wang ◽  
Zhi‐cheng Jing ◽  
Ping Ma ◽  
Qing‐bing Xu ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
In Vitro Studies ◽  
Protective Effects ◽  
Pulmonary Arterial
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