Lung Injury: Smoke-Induced https://greenmedinfo.com/taxonomy/term/62444/all en Epigallocatechin gallate diminishes cigarette smoke-induced oxidative stress, lipid peroxidation, and inflammation in human bronchial epithelial cells. https://greenmedinfo.com/article/epigallocatechin-gallate-diminishes-cigarette-smoke-induced-oxidative-stress-l PMID:  Life Sci. 2020 Aug 12:118260. Epub 2020 Aug 12. PMID: 32795541 Abstract Title:  Epigallocatechin gallate diminishes cigarette smoke-induced oxidative stress, lipid peroxidation, and inflammation in human bronchial epithelial cells. Abstract:  Cigarette smoke (CS), the major risk factor of chronic obstructive pulmonary disease (COPD), contains numerous free radicals that can cause oxidative stress and exaggerated inflammatory responses in the respiratory system. Lipid peroxidation which is oxidative degradation of polyunsaturated fatty acids and results in cell damage has also been associated with COPD pathogenesis. Increased levels of lipid peroxidation as well as its end product 4-hydroxynonenal have indeed been detected in COPD patients. Additionally, reactive oxygen species such as those contained in CS can activate nuclear factor-κB signaling pathway, initiating cascades of proinflammatory mediator expression. As emerging evidence attests to the antioxidative and anti-inflammatory properties of tea catechins, we sought to determine whether epigallocatechin gallate, the most abundant tea catechin, can provide protection against oxidative stress, lipid peroxidation, and inflammatory responses caused by CS. We found that EGCG treatment blocked cigarette smoke extract (CSE)-induced oxidative stress as indicated by decreased production and accumulation of reactive oxygen species in airway epithelial cells (AECs). Likewise,lipid peroxidation in CSE-stimulated AECs was suppressed by EGCG. Our findings further suggest that EGCG sequestered 4-hydroxynonenal and interfered with its protein adduct formation. Lastly, we show that EGCG inhibited nuclear factor-κB activation and the downstream expression of proinflammatorymediators. In summary, our study describing the antioxidative and anti-inflammatory effects of EGCG in CSE-exposed AECs provide valuable information about the therapeutic potential of this tea catechin for COPD. <p><a href="https://greenmedinfo.com/article/epigallocatechin-gallate-diminishes-cigarette-smoke-induced-oxidative-stress-l" target="_blank">read more</a></p> https://greenmedinfo.com/article/epigallocatechin-gallate-diminishes-cigarette-smoke-induced-oxidative-stress-l#comments EGCG (Epigallocatechin gallate) Lung Injury: Smoke-Induced Anti-Inflammatory Agents Antioxidants In Vitro Study Tue, 25 Aug 2020 15:46:48 +0000 greenmedinfo 225791 at https://greenmedinfo.com Alantolactone suppresses inflammation, apoptosis and oxidative stress in cigarette smoke-induced human bronchial epithelial cells. https://greenmedinfo.com/article/alantolactone-suppresses-inflammation-apoptosis-and-oxidative-stress-cigarette PMID:  Respir Res. 2020 Apr 22 ;21(1):95. Epub 2020 Apr 22. PMID: 32321531 Abstract Title:  Alantolactone suppresses inflammation, apoptosis and oxidative stress in cigarette smoke-induced human bronchial epithelial cells through activation of Nrf2/HO-1 and inhibition of the NF-κB pathways. Abstract:  BACKGROUND: It is well established that airway remodeling and inflammation are characteristics for chronic obstructive pulmonary disease (COPD). Moreover, cigarette smoke extract (CSE) promots inflammation, apoptosis and oxidative stress in COPD. And, there is evidence suggested that alantolactone (ALT), a sesquiterpene lactone isolated from Inula helenium, plays an adverse role in inflammation, apoptosis and oxidative stress. However, few studies have investigated the function and mechanism of ALT treatment on the COPD pathological process.METHODS: The levels of IL-1β, TNF-α, IL-6 and IFN-γ were examined by ELISA. Cells&#039; apoptosis and caspase-3 activity were detected by Cell Death Detection PLUS enzyme-linked immunosorbent assay and caspase-Glo 3/7 Assay, respectively. The content of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by using MDA and SOD assay kits. Reactive oxygen species (ROS) generation was measured by DCFH-DA assay. Protein expression was assayed by Western blot.RESULTS: In the present study, we aimed to observe the protective effects of ALT against inflammation, apoptosis and oxidative stress in human bronchial epithelial Beas-2B and NHBE cells. Our results showed that different doses of CSE exposure induced Beas-2B and NHBE cell inflammatory cytokines IL-1β, TNF-α, IL-6 and IFN-γ expression, cell apoptosis, caspase-3 activity and mediated oxidative stress markers MDA, ROS and SOD levels, while ALT treatment counteracted the effects of CSE. Further studies suggested that ALT attenuated NF-κB pathway activation. ALT also activated the Nrf2/HO-1 signal pathway through promoting Nrf2 nuclear aggregation and downstream HO-1 protein expression. HO-1 inhibitor tin protoporphyrin IX (SnPP IX) reversed the effects of ALT on Beas-2B and NHBE cell inflammation, apoptosis and oxidative stress.CONCLUSIONS: The above results collectively suggested that ALT suppressed CSE-induced inflammation, apoptosis and oxidative stress by modulating the NF-ĸB and Nrf2/ HO-1 axis. <p><a href="https://greenmedinfo.com/article/alantolactone-suppresses-inflammation-apoptosis-and-oxidative-stress-cigarette" target="_blank">read more</a></p> https://greenmedinfo.com/article/alantolactone-suppresses-inflammation-apoptosis-and-oxidative-stress-cigarette#comments Elecampane Lung Injury: Smoke-Induced Oxidative Stress Anti-Inflammatory Agents Antioxidants Apoptotic Heme oxygenase-1 up-regulation NF-kappaB Inhibitor Nrf2 activation In Vitro Study Thu, 30 Sep 2021 19:37:09 +0000 greenmedinfo 246573 at https://greenmedinfo.com Andrographolide protects against cigarette smoke-induced lung inflammation through activation of heme oxygenase-1. https://greenmedinfo.com/article/andrographolide-protects-against-cigarette-smoke-induced-lung-inflammation-thr PMID:  J Biochem Mol Toxicol. 2013 May ;27(5):259-65. Epub 2013 Apr 29. PMID: 23629921 Abstract Title:  Andrographolide protects against cigarette smoke-induced lung inflammation through activation of heme oxygenase-1. Abstract:  This study was conducted to check whether andrographolide, a bioactive molecule isolated from Andrographis paniculata, could protect against cigarette smoke (CS)-induced lung injury through activation of heme oxygenase-1 (HO-1). Pretreatment with andrographolide (1 mg/kg body weight) markedly attenuated lung inflammation in CS-exposed mice, coupled with reduced numbers of total cells, neutrophils, and macrophages in bronchial alveolar lavage fluid (BALF) and decreased production of cytokine/chemokine into BALF. Furthermore, andrographolide pretreatment increased the expression and activation of HO-1 in the lung of CS-exposed animals. Notably, these histological and biochemical changes induced by andrographolide were blocked by prior administration of zinc protoporphyrin IX (ZnPP; 20 mg/kg body weight), a potent heme oxygenase inhibitor. Moreover, andrographolide-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3) was attenuated by ZnPP treatment in CS-exposed animals. Our data collectively demonstrate that andrographolide confers protection against CS-induced lung inflammation, partially through activation of HO-1 and STAT3. <p><a href="https://greenmedinfo.com/article/andrographolide-protects-against-cigarette-smoke-induced-lung-inflammation-thr" target="_blank">read more</a></p> https://greenmedinfo.com/article/andrographolide-protects-against-cigarette-smoke-induced-lung-inflammation-thr#comments Andrographolide Lung Injury: Smoke-Induced Anti-Inflammatory Agents Heme oxygenase-1 up-regulation Animal Study Sat, 07 Aug 2021 23:54:45 +0000 greenmedinfo 243983 at https://greenmedinfo.com Antrodia camphorata may be useful for prevention of cigarette smoke-induced oxidative stress and diseases. https://greenmedinfo.com/article/antrodia-camphorata-may-be-useful-prevention-cigarette-smoke-induced-oxidative PMID:  Environ Toxicol. 2017 Aug ;32(8):2070-2084. Epub 2017 Apr 3. PMID: 28370894 Abstract Title:  Antrodia camphorata attenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice. Abstract:  Cigarette smoke exposure activates several cellular mechanisms predisposing to atherosclerosis, including oxidative stress, dyslipidemia, and vascular inflammation. Antrodia camphorata, a renowned medicinal mushroom in Taiwan, has been investigated for its antioxidant, anti-inflammatory, and antiatherosclerotic properties in cigarette smoke extracts (CSE)-treated vascular smooth muscle cells (SMCs), and ApoE-deficient mice. Fermented culture broth of Antrodia camphorata (AC, 200-800µg/mL) possesses effective antioxidant activity against CSE-induced ROS production. Treatment of SMCs (A7r5) with AC (30-120 µg/mL) remarkably ameliorated CSE-induced morphological aberrations and cell death. Suppressed ROS levels by AC corroborate with substantial inhibition of CSE-induced DNA damage in AC-treated A7r5 cells. We found CSE-induced apoptosis through increased Bax/Bcl-2 ratio, was substantially inhibited by AC in A7r5 cells. Notably, upregulated SOD and catalase expressions in AC-treated A7r5 cells perhaps contributed to eradicate the CSE-induced ROS generation, and prevents DNA damage and apoptosis. Besides, AC suppressed AP-1 activity by inhibiting the c-Fos/c-Jun expressions, and NF-κB activation through inhibition of I-κBα degradation against CSE-stimulation. This anti-inflammatory property of AC was accompanied by suppressed CSE-induced VEGF, PDGF, and EGR-1 overexpressions in A7r5 cells. Furthermore, AC protects lung fibroblast (MRC-5) cells from CSE-induced cell death. In vivo data showed that AC oral administration (0.6 mg/d/8-wk) prevents CSE-accelerated atherosclerosis in ApoE-deficient mice. This antiatherosclerotic property was associated with increased serum total antioxidant status, and decreased total cholesterol and triacylglycerol levels. Thus, Antrodia camphorata may be useful for prevention of CSE-induced oxidative stress and diseases. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2070-2084, 2017. <p><a href="https://greenmedinfo.com/article/antrodia-camphorata-may-be-useful-prevention-cigarette-smoke-induced-oxidative" target="_blank">read more</a></p> https://greenmedinfo.com/article/antrodia-camphorata-may-be-useful-prevention-cigarette-smoke-induced-oxidative#comments Antrodia camphorata Atherosclerosis DNA damage Inflammation Lung Injury: Smoke-Induced Oxidative Stress Anti-Apoptotic Anti-Inflammatory Agents Antioxidants NF-kappaB Inhibitor In Vitro Study Mon, 14 May 2018 21:03:23 +0000 greenmedinfo 164220 at https://greenmedinfo.com Cigarette smoke exposure impairs pulmonary bacterial clearance and alveolar macrophage complement-mediated phagocytosis of Streptococcus pneumoniae. https://greenmedinfo.com/article/cigarette-smoke-exposure-impairs-pulmonary-bacterial-clearance-and-alveolar-ma PMID:  Infect Immun. 2010 Mar ;78(3):1214-20. Epub 2009 Dec 14. PMID: 20008540 Abstract Title:  Cigarette smoke exposure impairs pulmonary bacterial clearance and alveolar macrophage complement-mediated phagocytosis of Streptococcus pneumoniae. Abstract:  Cigarette smoke exposure increases the risk of pulmonary and invasive infections caused by Streptococcus pneumoniae, the most commonly isolated organism from patients with community-acquired pneumonia. Despite this association, the mechanisms by which cigarette smoke exposure diminishes host defense against S. pneumoniae infections are poorly understood. In this study, we compared the responses of BALB/c mice following an intratracheal challenge with S. pneumoniae after 5 weeks of exposure to room air or cigarette smoke in a whole-body exposure chamber in vivo and the effects of cigarette smoke on alveolar macrophage phagocytosis of S. pneumoniae in vitro. Bacterial burdens in cigarette smoke-exposed mice were increased at 24 and 48 h postinfection, and this was accompanied by a more pronounced clinical appearance of illness, hypothermia, and increased lung homogenate cytokines interleukin-1beta (IL-1beta), IL-6, IL-10, and tumor necrosis factor alpha (TNF-alpha). We also found greater numbers of neutrophils in bronchoalveolar lavage fluid recovered from cigarette smoke-exposed mice following a challenge with heat-killed S. pneumoniae. Interestingly, overnight culture of alveolar macrophages with 1% cigarette smoke extract, a level that did not affect alveolar macrophage viability, reduced complement-mediated phagocytosis of S. pneumoniae, while the ingestion of unopsonized bacteria or IgG-coated microspheres was not affected. This murine model provides robust additional support to the hypothesis that cigarette smoke exposure increases the risk of pneumococcal pneumonia and defines a novel cellular mechanism to help explain this immunosuppressive effect. <p><a href="https://greenmedinfo.com/article/cigarette-smoke-exposure-impairs-pulmonary-bacterial-clearance-and-alveolar-ma" target="_blank">read more</a></p> https://greenmedinfo.com/article/cigarette-smoke-exposure-impairs-pulmonary-bacterial-clearance-and-alveolar-ma#comments Lung Inflammation Lung Injury: Smoke-Induced Pneumococcal Infections Risk Factors Animal Study Wed, 19 Feb 2020 15:07:04 +0000 greenmedinfo 212515 at https://greenmedinfo.com Diallyl disulfide prevents cigarette smoke-induced emphysema. https://greenmedinfo.com/article/diallyl-disulfide-prevents-cigarette-smoke-induced-emphysema PMID:  Pulm Pharmacol Ther. 2021 Aug ;69:102053. Epub 2021 Jul 5. PMID: 34214692 Abstract Title:  Diallyl disulfide prevents cigarette smoke-induced emphysema in mice. Abstract:  INTRODUCTION: Cigarette smoke (CS) is the main risk factor for the development of chronic obstructive pulmonary disease (COPD) and pulmonary emphysema. The use of antioxidants has emerged as a potential therapeutic strategy to treat airway inflammation and lung diseases. In the current study, we investigated the potential therapeutic impact of diallyl disulfide (Dads) treatment in a murine model of CS-induced emphysema.METHODS: C57BL/6 mice were exposed to CS for 60 consecutive days and treated with vehicle or Dads (30, 60 or 90 mg/kg) by oral gavage for the last 30 days, three times/week. The control group was sham-smoked and received vehicle treatment. All mice were euthanized 24 h after day 60; bronchoalveolar lavage (BAL) was performed and lungs were processed for further experimentation. Histological (HE stained sections, assessment of mean linear intercept (Lm)), biochemical (nitrite, superoxide dismutase (SOD), glutathione transferase (GST), and malondialdehyde (MDA) equivalents), and molecular biology (metalloproteinase (MMP) 12, SOD2, carbonyl reductase 1 (CBR1), nitrotyrosine (PNK), 4-hydroxynonenal (4-HNE), and CYP2E1) analyses were performed.RESULTS: Treatment with Dads dose-dependently reduced CS-induced leukocyte infiltration into the airways (based on BAL fluid counts) and improved lung histology (indicated by a reduction of Lm). Furthermore, CS exposure dramatically reduced the activity of the antioxidant enzymes SOD and GST in lung tissue and increased nitrite and MDA levels in BAL; these effects were all effectively counteracted by Dads treatment. Western blot analysis further confirmed the antioxidant potential of Dads, showing that treatment prevented the CS-induced decrease in SOD2 expression and increase in lung damage markers, such as CBR1, PNK, and 4-HNE. Furthermore, increased MMP12 (an important hallmark of CS-induced emphysema) and CYP2E1 lung protein levels were significantly reduced in mice receiving Dads treatment.CONCLUSION: Our findings demonstrate that treatment with Dads is effective in preventing multiple pathological features of CS-induced emphysema in an in vivo mouse model. In addition, we have identified several proteins/enzymes, including 4-HNE, CBR1, and CYP2E1, that are modifiable by Dads and could represent specific therapeutic targets for the treatment of COPD and emphysema. <p><a href="https://greenmedinfo.com/article/diallyl-disulfide-prevents-cigarette-smoke-induced-emphysema" target="_blank">read more</a></p> https://greenmedinfo.com/article/diallyl-disulfide-prevents-cigarette-smoke-induced-emphysema#comments Emphysema: Pulmonary Garlic Lung Injury: Smoke-Induced Organosulfur Compounds Anti-Inflammatory Agents Antioxidants Enzyme Activators Animal Study Thu, 09 Sep 2021 22:10:43 +0000 greenmedinfo 245565 at https://greenmedinfo.com Effect of piperlongumine during exposure to cigarette smoke reduces inflammation and lung injury. https://greenmedinfo.com/article/effect-piperlongumine-during-exposure-cigarette-smoke-reduces-inflammation-and PMID:  Pulm Pharmacol Ther. 2020 Jan 24 ;61:101896. Epub 2020 Jan 24. PMID: 31988027 Abstract Title:  Effect of piperlongumine during exposure to cigarette smoke reduces inflammation and lung injury. Abstract:  Chronic obstructive pulmonary disease (COPD) is related to smoking and anti-inflammatory therapy is indicated. Among the mediators with anti-inflammatory properties, we highlight piperlongumine (PL), an alkaloid/amide of Piper longum. Here we evaluated the PL administration on an experimental model of respiratory inflammation resulting from exposure to cigarette smoke. Male Balb/c mice were exposed to burning of 10 commercial cigarettes, 2x/day, for five weeks on specific equipment. PL efficacy was evaluated in control, exposed to smoke without treatment and PL treated (2.0 mg/kg, 3x/week) groups. Animals were weighed and plethysmographic analyses performed at the end of the exposure protocol. Inflammatory cells were evaluated in the bronchoalveolar lavage (BAL) and hemoglobin and glucose in the blood. Lung fragments were processed for histopathological studies and AnxA1, COX-2, NF-kB and neutrophil elastase expressions. Plethysmography revealed that PL maintained pulmonary frequency, volume and ventilation parameters similar to controls, with respiratory volume reduction compared to untreated animals. Final weight was reduced in both exposed groups. PL decreased hemoglobin concentration, attenuated the reduction of glucose levels and reduced influx of lymphocytes, neutrophils and macrophages in BAL. Histopathologically occured infiltration of inflammatory cells, increase of the interalveolar septa and intra-alveolar spaces in untreated animals. But, PL administration recovered lung tissues and, immunohistochemically, promoted increased expression of AnxA1 and reduction of COX-2, NF-kB and neutrophil elastase. Together the results indicate that PL attenuates systemic and pulmonary inflammatory changes, partially by modulating the expression the endogenous AnxA1, and may represent a promising therapy in preventing the inflammation induced by cigarette smoke. <p><a href="https://greenmedinfo.com/article/effect-piperlongumine-during-exposure-cigarette-smoke-reduces-inflammation-and" target="_blank">read more</a></p> https://greenmedinfo.com/article/effect-piperlongumine-during-exposure-cigarette-smoke-reduces-inflammation-and#comments Chronic Obstructive Pulmonary Disease Lung Damage Lung Inflammation Lung Injury: Smoke-Induced Piperlongumine Anti-Inflammatory Agents Cyclooxygenase 2 Inhibitors NF-kappaB Inhibitor In Vitro Study Mon, 17 Feb 2020 01:58:17 +0000 greenmedinfo 212210 at https://greenmedinfo.com Fisetin alleviates cigarette smoke-induced oxidative stress and lung inflammation. https://greenmedinfo.com/article/fisetin-alleviates-cigarette-smoke-induced-oxidative-stress-and-lung-inflammat PMID:  J Food Biochem. 2019 Aug ;43(8):e12962. Epub 2019 Jun 28. PMID: 31368542 Abstract Title:  The plant flavonoid, fisetin alleviates cigarette smoke-induced oxidative stress, and inflammation in Wistar rat lungs. Abstract:  In the present study, we tested the antioxidant and anti-inflammatory potential of the plant flavonoid, fisetin against cigarette smoke-induced oxidative stress, and inflammation in rat lungs. Male Wistar rats were chronically exposed to cigarette smoke (CS) with or without administration of fisetin. Fisetin administration to CS-exposed rats resulted in a significant reduction in neutrophils and macrophages in bronchoalveolar lavage fluid as well as malondialdehyde, 3-nitrotyrosine, 8-isoprostane, tumor necrosis factor-alpha, interleukin-1beta, granulocyte macrophage-colony stimulating factor, interleukin-4, and interleukin-10 levels in lung tissues compared to those in CS-exposed rats not treated with fisetin. Fisetin also significantly augmented lung hemoxinase-1, glutathione peroxidase-2, reduced glutathione, superoxide dismutase, nitric oxide, and nuclear factor erythroid 2-related factor (Nrf2) levels in CS-exposed rats. In addition, a marked reversal in CS-induced histopathological changes was noted in fisetin-treated rats. Collectively, these data demonstrate the potential of fisetin to blunt CS-induced oxidative stress and inflammation in the lung and to prevent tissue damage via the Nrf2-mediated upregulation of antioxidant gene expression. PRACTICAL APPLICATIONS: In the present study, we found that the plant flavonoid, fisetin significantly abrogated the oxidative stress, inflammation, and tissue damage induced by cigarette smoke, a powerful pro-oxidant in rat lungs. Additionally, fisetin markedly reversed cigarette smoke-induced increases in neutrophil and macrophage cell populations in bronchoalveolar lavage fluid. These findings are particularly significant considering the association of cigarette smoking with increased oxidative stress and inflammation, which are central to the pathologies of a wide variety of chronic diseases including chronic obstructive pulmonary disease, cancer, and cardiovascular diseases. Therefore, the present work underscores the beneficial effects of the regular consumption of plant-based foods with medicinal properties for the effective prevention of these chronic diseases. <p><a href="https://greenmedinfo.com/article/fisetin-alleviates-cigarette-smoke-induced-oxidative-stress-and-lung-inflammat" target="_blank">read more</a></p> https://greenmedinfo.com/article/fisetin-alleviates-cigarette-smoke-induced-oxidative-stress-and-lung-inflammat#comments Fisetin Lung Inflammation Lung Injury: Smoke-Induced Anti-Inflammatory Agents Antioxidants Nrf2 activation In Vitro Study Wed, 18 Dec 2019 02:34:15 +0000 greenmedinfo 205375 at https://greenmedinfo.com Ginsenoside Rb3 exerts protective properties against cigarette smoke extract-induced cell injury. https://greenmedinfo.com/article/ginsenoside-rb3-exerts-protective-properties-against-cigarette-smoke-extract-i PMID:  Biomed Pharmacother. 2018 Oct 12 ;108:1751-1758. Epub 2018 Oct 12. PMID: 30372878 Abstract Title:  Ginsenoside Rb3 exerts protective properties against cigarette smoke extract-induced cell injury by inhibiting the p38 MAPK/NF-κB and TGF-β1/VEGF pathways in fibroblasts and epithelial cells. Abstract:  Cigarette smoke causes many adverse effects such as inflammation, oxidative stress, and excessive accumulation of the extracellular matrix (ECM). Ginsenoside Rb3 has anti-inflammatory and anti-oxidative effects, which may contribute to delaying the injury caused by cigarette smoke. In this study, we used cigarette smoke extract (CSE) to establish cell injury models in WI-38 human fetal lung fibroblasts and 16HBE human bronchial epithelial cells. Our results showed that Rb3 protected against CSE-induced cytotoxicity in both cell lines. In addition, it significantly inhibited the secretion of inflammatory factors, such as interleukin-8 and tumor necrosis factor alpha, by inhibiting the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB). Moreover, Rb3 pre-treatment led to an increase in the levels of glutathione (GSH) and activities of superoxide dismutase, glutathione peroxidase (GSH-Px), and catalase to reduce the oxidative stress induced by CSE. Additionally, Rb3 decreased the levels of ECM proteins including collagen I (Col I), Col III, and elastin after CSE treatment by inhibiting the expression of transforming growth factor beta 1 (TGF-β1)-induced vascular endothelial growth factor (VEGF). Our findings suggest that Rb3 prevented CSE-induced inflammation and oxidative stress as well as the excessive accumulation ofECM in WI-38 and 16HBE cells to protect against cell injury by inhibiting the p38 MAPK/NF-κB and TGF-β1/VEGF pathways. The results of this study may be valuable for the development of Rb3 to combat the damage caused by cigarette smoke. <p><a href="https://greenmedinfo.com/article/ginsenoside-rb3-exerts-protective-properties-against-cigarette-smoke-extract-i" target="_blank">read more</a></p> https://greenmedinfo.com/article/ginsenoside-rb3-exerts-protective-properties-against-cigarette-smoke-extract-i#comments Ginsenosides Lung Injury: Smoke-Induced Anti-Inflammatory Agents Interleukin-8 downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Sat, 03 Nov 2018 03:01:45 +0000 greenmedinfo 173408 at https://greenmedinfo.com Ginsenoside Rg1 attenuates cigarette smoke-induced pulmonary epithelial-mesenchymal transition. https://greenmedinfo.com/article/ginsenoside-rg1-attenuates-cigarette-smoke-induced-pulmonary-epithelial-mesenc PMID:  Biomed Res Int. 2017 ;2017:7171404. Epub 2017 Aug 13. PMID: 29104873 Abstract Title:  Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-1/Smad Pathway. Abstract:  Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction.is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS) and human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE). Our data showed that CS or CSE exposure increased expression of the mesenchymal marker-smooth muscle actin (-SMA) and decreased expression of the epithelial marker epithelial cadherin (E-cad) in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-1/Smad pathway components, including TGF-1, TGF-R1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-R1-Smad2/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-1/Smad pathway. <p><a href="https://greenmedinfo.com/article/ginsenoside-rg1-attenuates-cigarette-smoke-induced-pulmonary-epithelial-mesenc" target="_blank">read more</a></p> https://greenmedinfo.com/article/ginsenoside-rg1-attenuates-cigarette-smoke-induced-pulmonary-epithelial-mesenc#comments Ginsenosides Lung Injury: Smoke-Induced Animal Study In Vitro Study Thu, 01 Mar 2018 22:18:22 +0000 greenmedinfo 160598 at https://greenmedinfo.com Ginsenoside Rg1 may suppress cigarette smoke-induced airway fibrosis in pulmonary fibroblasts and COPD rats. https://greenmedinfo.com/article/ginsenoside-rg1-may-suppress-cigarette-smoke-induced-airway-fibrosis-pulmonary n/a PMID:  Biomed Res Int. 2017 ;2017:6510198. Epub 2017 Mar 21. PMID: 28421197 Abstract Title:  Ginsenoside Rg1 Ameliorates Cigarette Smoke-Induced Airway Fibrosis by Suppressing the TGF-β1/Smad Pathway In Vivo and In Vitro. Abstract:  Small airway fibrosis is a key pathological process accompanying chronic obstructive pulmonary disease (COPD) and includes fibroblast/myofibroblast transdifferentiation and excessive extracellular matrix deposition. Ginsenoside Rg1, one of the main active ingredients of Panax ginseng, has been shown to exert an antifibrotic effect in many tissues. However, little is known about the underlying mechanism and whether ginsenoside Rg1 can exert an effect on small airway fibrosis. We investigated the anti-small airway fibrosis effects of ginsenoside Rg1 in human embryonic lung fibroblasts and in COPD rats. We found that ginsenoside Rg1 effectively reduced the degree of pulmonary fibrosis, decreased the expression ofα-smooth muscle actin, collagen I, and matrix metalloproteinase 9, and maintained the ratio of matrix metalloproteinase 9 to tissue inhibitor of metalloproteinase 1. Importantly, ginsenoside Rg1 significantly attenuated cigarette smoke extract-induced upregulation of transforming growth factor β1,TGF-β receptor I, phospho-Smad2, and phospho-Smad3. In addition, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-β receptor I-Smad2/3 inhibitor. Collectively, these results suggest that ginsenoside Rg1 may suppress cigarette smoke-induced airway fibrosis in pulmonary fibroblasts and COPD rats by inhibiting the TGF-β1/Smad signaling pathway. https://greenmedinfo.com/article/ginsenoside-rg1-may-suppress-cigarette-smoke-induced-airway-fibrosis-pulmonary#comments Chronic Obstructive Pulmonary Disease Ginsenosides Lung Injury: Smoke-Induced Smoking: Pulmonary Anti-Fibrotic Anti-Fibrotic Chronic Obstructive Pulmonary Disease Ginsenosides Lung Injury: Smoke-Induced Smoking: Pulmonary Animal Study In Vitro Study Fri, 12 May 2017 21:02:26 +0000 greenmedinfo 147679 at https://greenmedinfo.com Ginsenoside Rg1 protects against cigarette smoke-induced airway remodeling. https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-cigarette-smoke-induced-airway-remodeling PMID:  Am J Transl Res. 2020 ;12(2):493-506. Epub 2020 Feb 15. PMID: 32194898 Abstract Title:  Ginsenoside Rg1 protects against cigarette smoke-induced airway remodeling by suppressing the TGF-β1/Smad3 signaling pathway. Abstract:  Chronic obstructive pulmonary disease (COPD) is a devastating and common respiratory disease characterized by chronic inflammation and progressive airway remodeling. Ginsenoside Rg1 (GRg1), a major active component of, has been found to possess beneficial properties against acute lung injury and respiratory diseases. However, the effects of GRg1 on airway remodeling in COPD remain unclear. In this study, we aimed to investigate the potential protective effects of GRg1 on airway remodeling induced by cigarette smoke (CS) and the underlying mechanism. A rat model of COPD was established in which the animals were subjected to CS and GRg1 daily for 12 weeks. Subsequently, we evaluated lung function, inflammatory responses, along with airway remodeling and associated signaling factors. GRg1 treatment was found to improve pulmonary function, reduce airway collagen volume fraction, and markedly reduce the expression of IL-6, TNF-α, α-SMA, and collagen I. Moreover, GRg1 treatment decreased the expression of TGF-β1, TGF-βR1, and phosphorylated-Smad3., pretreatment of MRC5 human lung fibroblasts with GRg1 prior to exposure to cigarette smoke extract (CSE) reversed the cell ultrastructure disorder, decreased the expression of IL-6 and TNF-α, and significantly attenuated transdifferentiation of MRC5 cells by suppressing α-SMA and collagen I expression. Additionally, GRg1 suppressed the TGF-β1/Smad3 signaling pathway in CSE-stimulated MRC5 cells, whereas Smad3 over-expression abolished the anti-transdifferentiation effect of GRg1. In conclusion, the results of our study demonstrated that GRg1 improves lung function and protects against CS-induced airway remodeling, in part by down-regulating the TGF-β1/Smad3 signaling pathway. <p><a href="https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-cigarette-smoke-induced-airway-remodeling" target="_blank">read more</a></p> https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-cigarette-smoke-induced-airway-remodeling#comments Ginsenosides Lung Injury: Smoke-Induced Anti-Inflammatory Agents Interleukin-6 Downregulation Transforming growth factor beta (TGF-β) inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Thu, 26 Mar 2020 12:47:12 +0000 greenmedinfo 217197 at https://greenmedinfo.com Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues. https://greenmedinfo.com/article/hesperidin-inhibits-tobacco-smoke-induced-pulmonary-cell-proliferation-and-emt PMID:  Oncol Lett. 2023 Jan ;25(1):30. Epub 2022 Nov 29. PMID: 36589667 Abstract Title:  Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway. Abstract:  Tobacco smoke (TS) is the major cause of lung cancer. The abnormal proliferation and epithelial-mesenchymal transition (EMT) of lung cells promote occurrence and development of lung cancer. The p38 pathway intervenes in this cancer development. Hesperidin also serves a role in human health and disease prevention. The roles of p38 in TS-mediated abnormal cell proliferation and EMT, and the hesperidin intervention thereof are not yet understood. In the present study, it was demonstrated that TS upregulated proliferating cell nuclear antigen, vimentin and N-cadherin expression, whereas it downregulated E-cadherin expression, as assessed using western blotting and reverse transcription-quantitative PCR. Furthermore, it was observed that inhibition of the p38 pathway inhibit TS-induced proliferation and EMT. Hesperidin treatment prevented the TS-induced activation of the p38 pathway, EMT and cell proliferation in mouse lungs. The findings of the present study may provide insights into the pathogenesis of TS-related lung cancer. <p><a href="https://greenmedinfo.com/article/hesperidin-inhibits-tobacco-smoke-induced-pulmonary-cell-proliferation-and-emt" target="_blank">read more</a></p> https://greenmedinfo.com/article/hesperidin-inhibits-tobacco-smoke-induced-pulmonary-cell-proliferation-and-emt#comments Hesperidin Lung Injury: Smoke-Induced Antiproliferative Animal Study Tue, 30 May 2023 20:00:17 +0000 greenmedinfo 273102 at https://greenmedinfo.com High-dose berberine ameliorated cigarette smoke extract-induced airway inflammation in COPD mice. https://greenmedinfo.com/article/high-dose-berberine-ameliorated-cigarette-smoke-extract-induced-airway-inflamm PMID:  Curr Med Sci. 2019 Oct ;39(5):748-753. Epub 2019 Oct 14. PMID: 31612392 Abstract Title:  Berberine Attenuates Cigarette Smoke Extract-induced Airway Inflammation in Mice: Involvement of TGF-β1/Smads Signaling Pathway. Abstract:  Although several studies confirmed that berberine may attenuate airway inflammation in mice with chronic obstructive pulmonary disease (COPD), its underlying mechanisms were not clear until now. We aimed to establish an experiment mouse model for COPD and to investigate the effects of berberine on airway inflammation and its possible mechanism in COPD model mice induced by cigarette smoke extract (CSE). Twenty SPF C57BL/6 mice were randomly divided into PBS control group, COPD model group, low-dose berberine group and high-dose berberine group, 5 mice in each group. The neutrophils and macrophages were examined by Wright&#039;s staining. The levels of inflammatory cytokines TNF-α and IL-6 in bronchoalveolar lavage fluid (BALF) were determined by enzyme-linked immunosorbent assay. The expression levels of TGF-β1, Smad2 and Smad3 mRNA and proteins in lung tissues were respectively detected by quantitative real-time polymerase chain reaction and Western blotting. It was found that CSE increased the number of inflammation cells in BALF, elevated lung inflammation scores, and enhanced the TGF-β1/Smads signaling activity in mice. High-dose berberine restrained the alterations in the COPD mice induced by CSE. It was concluded that high-dose berberine ameliorated CSE-induced airway inflammation in COPD mice. TGF-β1/Smads signaling pathway might be involved in the mechanism. These findings suggested a therapeutic potential of high-dose berberine on the CSE-induced airway inflammation. <p><a href="https://greenmedinfo.com/article/high-dose-berberine-ameliorated-cigarette-smoke-extract-induced-airway-inflamm" target="_blank">read more</a></p> https://greenmedinfo.com/article/high-dose-berberine-ameliorated-cigarette-smoke-extract-induced-airway-inflamm#comments Chronic Obstructive Pulmonary Disease Lung Injury: Smoke-Induced Pomegranate Anti-Inflammatory Agents Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Sun, 20 Oct 2019 19:49:16 +0000 greenmedinfo 199586 at https://greenmedinfo.com Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression. https://greenmedinfo.com/article/inhibition-oxidative-stress-apocynin-attenuated-chronic-obstructive-pulmonary- PMID:  Br J Pharmacol. 2023 Mar 12. Epub 2023 Mar 12. PMID: 36908040 Abstract Title:  Inhibition of oxidative stress by apocynin attenuated chronic obstructive pulmonary disease progression and vascular injury by cigarette smoke exposure. Abstract:  BACKGROUND AND PURPOSE: Cardiovascular disease affects up to half of the patients with chronic obstructive pulmonary disease (COPD), exerting deleterious impact on health outcomes and survivability. Vascular endothelial dysfunction marks the onset of cardiovascular disease. The present study examined the effect of a potent NADPH Oxidase (NOX) inhibitor and free-radical scavenger, apocynin, on COPD-related cardiovascular disease.EXPERIMENTAL APPROACH: Male BALB/c mice were exposed to either room air (Sham) or cigarette smoke (CS) generated from 9 cigarettes·day, 5 days a week for up to 24 weeks with or without apocynin treatment (5 mg·kg·day, intraperitoneal injection).KEY RESULTS: Eight-weeks of apocynin treatment reduced airway neutrophil infiltration (by 42%) and completely preserved endothelial function and endothelial nitric oxide synthase (eNOS) availability against the oxidative insults of cigarette smoke exposure. These preservative effects were maintained up until the 24-week time point. 24-week of apocynin treatment markedly reduced airway inflammation (reduced infiltration of macrophage, neutrophil and lymphocyte), lung function decline (hyperinflation) and prevented airway collagen deposition by cigarette smoke exposure.CONCLUSION AND IMPLICATIONS: Limiting NOX activity may slow COPD progression and lower cardiovascular disease risk, particularly when signs of oxidative stress become evident. <p><a href="https://greenmedinfo.com/article/inhibition-oxidative-stress-apocynin-attenuated-chronic-obstructive-pulmonary-" target="_blank">read more</a></p> https://greenmedinfo.com/article/inhibition-oxidative-stress-apocynin-attenuated-chronic-obstructive-pulmonary-#comments Apocynin Chronic Obstructive Pulmonary Disease Lung Injury: Smoke-Induced Anti-Inflammatory Agents Animal Study Tue, 13 Jun 2023 01:04:58 +0000 greenmedinfo 274712 at https://greenmedinfo.com