Effects Of Chinese Green Tea On Cigarette Smoke-induced Lung Inflammation, Oxidative Stress And Protease Activity In Rats

2010 ◽  
Author(s):  
Ka H. Chan ◽  
Sze C. Yeung ◽  
Mary S. Ip ◽  
Ricky Y.K. Man ◽  
Judith C. Mak
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Green Tea ◽  
Lung Inflammation ◽  
Protease Activity

Eucalyptol attenuates cigarette smoke-induced acute lung inflammation and oxidative stress in the mouse

2016 ◽  
Vol 41 ◽  
pp. 11-18 ◽  
Author(s):  
Emanuel Kennedy-Feitosa ◽  
Renata Tiemi Okuro ◽  
Vanessa Pinho Ribeiro ◽  
Manuella Lanzetti ◽  
Marina Valente Barroso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Acute Lung Inflammation ◽  
And Oxidative Stress

scholarly journals Paeonol Attenuates Cigarette Smoke-Induced Lung Inflammation by Inhibiting ROS-Sensitive Inflammatory Signaling

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Meng-Han Liu ◽  
An-Hsuan Lin ◽  
Hung-Fu Lee ◽  
Hsin-Kuo Ko ◽  
Tzong-Shyuan Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Chinese Herb ◽  
Inflammatory Infiltration ◽  
Beneficial Effects ◽  
Antioxidant Function ◽  
Mitogen Activated Protein

Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have previously reported that cigarette smoke (CS) activates reactive oxygen species- (ROS-) sensitive mitogen-activated protein kinases (MAPKs)/nuclear factor-κB (NF-κB) signaling leading to induction of lung inflammation. Paeonol, the main phenolic compound present in the Chinese herbPaeonia suffruticosa, has antioxidant and anti-inflammatory properties. However, whether paeonol has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model, we showed that chronic CS exposure for 4 weeks caused pulmonary inflammatory infiltration, increased lung vascular permeability, elevated lung levels of chemokines, cytokines, and 4-hydroxynonenal (an oxidative stress biomarker), and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with paeonol. Using human bronchial epithelial cells (HBECs), we demonstrated that cigarette smoke extract (CSE) sequentially increased extracellular and intracellular levels of ROS, activated the MAPKs/NF-κB signaling, and induced interleukin-8 (IL-8); all these CSE-induced events were inhibited by paeonol pretreatment. Our findings suggest a novel role for paeonol in alleviating the oxidative stress and lung inflammation induced by chronic CS exposurein vivoand in suppressing CSE-induced IL-8in vitrovia its antioxidant function and an inhibition of the MAPKs/NF-κB signaling.

scholarly journals SIRT1 protects against cigarette smoke-induced lung oxidative stress via a FOXO3-dependent mechanism

2014 ◽  
Vol 306 (9) ◽  
pp. L816-L828 ◽  
Author(s):  
Hongwei Yao ◽  
Isaac K. Sundar ◽  
Tanveer Ahmad ◽  
Chad Lerner ◽  
Janice Gerloff ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Subsequent Development ◽  
Chronic Obstructive ◽  
Heme Oxygenase 1 ◽  
Quinone Oxidoreductase ◽  
Deficient Mice ◽  
Lung Oxidative Stress

Oxidative and carbonyl stress is increased in lungs of smokers and patients with chronic obstructive pulmonary disease (COPD), as well as in cigarette smoke (CS)-exposed rodent lungs. We previously showed that sirtuin1 (SIRT1), an antiaging protein, is reduced in lungs of CS-exposed mice and patients with COPD and that SIRT1 attenuates CS-induced lung inflammation and injury. It is not clear whether SIRT1 protects against CS-induced lung oxidative stress. Therefore, we determined the effect of SIRT1 on lung oxidative stress and antioxidants in response to CS exposure using loss- and gain-of-function approaches, as well as a pharmacological SIRT1 activation by SRT1720. We found that CS exposure increased protein oxidation and lipid peroxidation in lungs of wild-type (WT) mice, which was further augmented in SIRT1-deficient mice. Furthermore, both SIRT1 genetic overexpression and SRT1720 treatment significantly decreased oxidative stress induced by CS exposure. FOXO3 deletion augmented lipid peroxidation products but reduced antioxidants in response to CS exposure, which was not affected by SRT1720. Interestingly, SRT1720 treatment exhibited a similar effect on lipid peroxidation and antioxidants (i.e., manganese superoxide dismutase, heme oxygenase-1, and NADPH quinone oxidoreductase-1) in WT and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-deficient mice in response to CS exposure. This indicates that SIRT1 protects against CS-induced oxidative stress, which is mediated by FOXO3, but is independent of Nrf2. Overall, these findings reveal a novel function of SIRT1, which is to reduce CS-induced oxidative stress, and this may contribute to its protective effects against lung inflammation and subsequent development of COPD.

scholarly journals Ebselen abolishes vascular dysfunction in influenza A virus-induced exacerbations of cigarette smoke-induced lung inflammation in mice

2021 ◽  
Author(s):  
Kurt Brassington ◽  
Stanley Chan ◽  
Simone De Luca ◽  
Aleksandar Dobric ◽  
Kevin Mou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cell ◽  
Cigarette Smoke ◽  
Influenza A Virus ◽  
Vascular Function ◽  
Lung Inflammation ◽  
Influenza A ◽  
Respiratory Infections ◽  
Vascular Dysfunction ◽  
Cardiovascular Complications

Background and Purpose: People with COPD are susceptible to respiratory infections which exacerbate pulmonary and/or cardiovascular complications, increasing their likelihood of death. The mechanisms driving these complications remain unknown but increased oxidative stress has been implicated. Here we investigated whether influenza A virus (IAV) infection, following chronic cigarette smoke (CS) exposure, worsens vascular function and if so, whether the antioxidant ebselen alleviates this vascular dysfunction. Experimental Approach: Male BALB/c mice were exposed to either room air or CS for 8 weeks followed by inoculation with IAV (Mem71, 1 x 104.5 pfu)). Mice were treated with ebselen (10 mg/kg) or vehicle (5% w/v CM-cellulose in water) daily. Mice were culled 3- and 10-days post-infection, and their lungs lavaged to assess inflammation. The thoracic aorta was excised to investigate endothelial and smooth muscle dilator responses, expression of key vasodilatory and oxidative stress modulators and infiltrating immune cells. Key Results: CS increased lung inflammation and caused significant vascular endothelial dysfunction, which was worsened by IAV infection. CS-driven increases in vascular oxidative stress and suppression of eNOS were not affected by IAV infection. CS and IAV infection significantly enhanced T-cell recruitment into the aortic wall. Ebselen abolished the exaggerated lung inflammation, vascular dysfunction and increased aortic T-cell infiltration in CS and IAV-infected mice. Conclusion and Implications: Ebselen abolished vascular dysfunction in IAV-induced exacerbations of cigarette smoke-induced lung inflammation indicating it may have potential for the treatment of cardiovascular comorbidities seen in acute exacerbations of COPD.

scholarly journals GAMBARAN HISTOPATOLOGI PARU PADA MENCIT (Mus musculus) YANG DIPAPAR ASAP ROKOK KRETEK AKIBAT PENGARUH PEMBERIAN INFUSA TEH HIJAU (Camellia sinensis)

2020 ◽  
Vol 10 ◽  
pp. 20-24
Author(s):  
Dyah Widhowati ◽  
Rondius Solfaine ◽  
Olan Rahayu Puji Astuti Mussa ◽  
Apriska Ayuningtias
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Green Tea ◽  
Camellia Sinensis ◽  
Ultrafine Particles ◽  
Visual Fields ◽  
Inflammatory Cells ◽  
Histological Structure ◽  
Tea Infusion ◽  
Biochemical Laboratory

This study was conducted to determine the effect of antioxidant administration from green tea infusion (Camellia sinensis) on damage to the histological structure of the lung exposed to clove cigarette smoke in mice (Mus muscullus). Free radicals in cigarette smoke such as tar, nicotine, and carbon monoxide can cause various damages to the lung or This study was conducted to determine the effect of antioxidant administration from green tea infusion (Camellia sinensis) on damage to the histological structure of the lung exposed to clove cigarette smoke in mice (Mus muscullus). Free radicals in cigarette smoke such as tar, nicotine, and carbon monoxide can cause various damages to the lung organs due to oxidative stress caused by the reaction of ultrafine particles with cells. A total of 27 mice were taken from the Biochemical Laboratory of Airlangga University, Surabaya. In this study mice (Mus muscullus) were exposed to kretek cigarette smoke in the smoking chamber for 15 minutes in a period of 2 weeks, used 2 variants of antioxidant doses of green tea infusion of 0.45 gr to 0.6 gr. After the treatment was completed, the preparation of the mice's pulmonary organ preparations and damage to the structure of the lung organ were observed in 9 visual fields. The results showed that there was a relationship between the amount of cigarette smoke exposed and damage to the lung organs of mice when given antioxidant green tea. The administration of green tea antioxidants reduced inflammation of the lung organ infiltration of inflammatory cells by 44%, edema by 55%, and destruction of septa alveoli by 88%. gans due to oxidative stress caused by the reaction of ultrafine particles with cells. A total of 27 mice were taken from the Biochemical Laboratory of Airlangga University, Surabaya. In this study mice (Mus muscullus) were exposed to kretek cigarette smoke in the smoking chamber for 15 minutes in a period of 2 weeks, used 2 variants of antioxidant doses of green tea infusion of 0.45 gr to 0.6 gr. After the treatment was completed, the preparation of the mice's pulmonary organ preparations and damage to the structure of the lung organ were observed in 9 visual fields. The results showed that there was a relationship between the amount of cigarette smoke exposed and damage to the lung organs of mice when given antioxidant green tea. The administration of green tea antioxidants reduced inflammation of the lung organ infiltration of inflammatory cells by 44%, edema by 55%, and destruction of septa alveoli by 88%.

Glutathione peroxidase-1 protects against cigarette smoke-induced lung inflammation in mice

2010 ◽  
Vol 299 (3) ◽  
pp. L425-L433 ◽  
Author(s):  
Chi Duong ◽  
Huei Jiunn Seow ◽  
Steven Bozinovski ◽  
Peter J. Crack ◽  
Gary P. Anderson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Protein Denaturation ◽  
Lung Damage ◽  
Glutathione Peroxidase 1 ◽  
Neutrophil Chemotactic Factor

Reactive oxygen species (ROS) produced from cigarette smoke cause oxidative lung damage including protein denaturation, lipid peroxidation, and DNA damage. Glutathione peroxidase-1 (gpx-1) is a detoxifying enzyme that may protect lungs from such damage. The aim of this study was to determine whether gpx-1 protects the lung against oxidative stress-induced lung inflammation in vivo. Male wild-type (WT) or gpx-1−/− mice were exposed to cigarette smoke generated from nine cigarettes per day for 4 days to induce oxidative stress and lung inflammation. The effect of the gpx mimetic ebselen on cigarette smoke-induced lung inflammation was evaluated when given prophylactically and therapeutically, i.e., during established inflammation. Mice were killed, and the lungs were lavaged with PBS and then harvested for genomic and proteomic analysis. Gpx-1−/− mice exposed to cigarette smoke had enhanced BALF neutrophils, macrophages, proteolytic burden, whole lung IL-17A, and MIP1α mRNA compared with WT mice. The gpx mimetic ebselen (10 and 100 μM) inhibited cigarette smoke extract-induced oxidation of MH-S cells in vitro and inhibited cigarette smoke-induced increases in BALF macrophages, neutrophils, proteolytic burden, and macrophage and neutrophil chemotactic factor gene expression when administered prophylactically. In addition, ebselen inhibited established BALF inflammation when administered therapeutically. These data show that gpx-1 protects against cigarette smoke-induced lung inflammation, and agents that mimic the actions of gpx-1 may have therapeutic utility in inflammatory lung diseases where cigarette smoke plays a role.

scholarly journals Neu-164 and Neu-107, two novel antioxidant and anti-myeloperoxidase compounds, inhibit acute cigarette smoke-induced lung inflammation

2013 ◽  
Vol 305 (2) ◽  
pp. L165-L174 ◽  
Author(s):  
Thomas H. Thatcher ◽  
Hsi-Min Hsiao ◽  
Elhanan Pinner ◽  
Moshe Laudon ◽  
Stephen J. Pollock ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lung Disease ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Inflammatory Cells ◽  
Oxygen Species ◽  
Acute Lung Inflammation ◽  
Antioxidant Genes ◽  
Endogenous Antioxidant

Cigarette smoke is a profound proinflammatory stimulus that causes acute lung inflammation and chronic lung disease, including chronic obstructive pulmonary disease (COPD, emphysema, and chronic bronchitis), via a variety of mechanisms, including oxidative stress. Cigarette smoke contains high levels of free radicals, whereas inflammatory cells, including macrophages and neutrophils, express enzymes, including NADPH oxidase, nitric oxide synthase, and myeloperoxidase, that generate reactive oxygen species in situ and contribute to inflammation and tissue damage. Neu-164 and Neu-107 are small-molecule inhibitors of myeloperoxidase, as well as potent antioxidants. We hypothesized that Neu-164 and Neu-107 would inhibit acute cigarette smoke-induced inflammation. Adult C57BL/6J mice were exposed to mainstream cigarette smoke for 3 days to induce acute inflammation and were treated daily by inhalation with Neu-164, Neu-107, or dexamethasone as a control. Inflammatory cells and cytokines were assessed by bronchoalveolar lavage and histology. mRNA levels of endogenous antioxidant genes heme oxygenase-1 and glutamate-cysteine ligase modifier subunit were determined by qPCR. Cigarette smoke exposure induced acute lung inflammation with accumulation of neutrophils and upregulation of proinflammatory cytokines, including IL-6, macrophage inflammatory protein-2, and keratinocyte-derived cytokine. Both Neu-164 and Neu-107 significantly reduced the accumulation of inflammatory cells and the expression of inflammatory cytokines as effectively as dexamethasone. Upregulation of endogenous antioxidant genes was dampened. Neu-164 and Neu-107 inhibit acute cigarette smoke-induced inflammation by scavenging reactive oxygen species in cigarette smoke and by inhibiting further oxidative stress caused by inflammatory cells. These compounds may have promise in preventing or treating lung disease associated with chronic smoke exposure, including COPD.

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