Cigarette smoke-mediated oxidative stress induces apoptosis via the MAPKs/STAT1 pathway in mouse lung fibroblasts

Lee, Hanbyeol; Park, Jeong-Ran; Kim, Eun-Jeong; Kim, Woo Jin; Hong, Seok‐Ho; Park, Sung Min; Yang, Se‐Ran

doi:10.1016/j.toxlet.2015.10.030

Cited by 55 publications

(45 citation statements)

References 47 publications

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“…A recent study showed CSE‐induced morphological alteration in lung fibroblasts characterized by loosened intracellular connections, membrane blebbing, and blunt nuclei. These adverse effects of CSE were accompanied with increased ROS‐mediated oxidative stress, inflammation, and apoptotic‐cell death . In our study, we found similar aberrant morphological features in both vascular SMCs and lung fibroblasts following CSE exposure.…”

Section: Discussionsupporting

confidence: 76%

“…Nicotine shown to produce ROS, which may trigger NF‐κB activation in rat mesencephalic cells . Besides, CSE‐induced ROS reported to decrease antioxidant status and activate inflammatory response, which may lead to death of lung fibroblasts through an imbalance between Bcl‐2 and Bax ratio . Paradoxically, smoking cessation or antioxidants treatment reported to decrease CSE‐induced atherogenic lipid profiles, inflammatory response (NF‐κB) and DNA damage .…”

Section: Introductionmentioning

confidence: 99%

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Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Yang

Korivi

Chen

et al. 2017

Environmental Toxicology

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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, 200-800 µg/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.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Yang

Korivi

Chen

et al. 2017

Environmental Toxicology

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“…CS extract (CSE) was prepared by using a modified method described by Lee et al (29). Research‐grade cigarettes (3R4F) were obtained from the Kentucky Tobacco Research Development Center (The Tobacco Research Institute, University of Kentucky, Lexington, KY, USA).…”

Section: Methodsmentioning

confidence: 99%

Blockade of RAGE ameliorates elastase‐induced emphysema development and progression via RAGE‐DAMP signaling

et al. 2017

Self Cite

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The receptor for advanced glycan end products (RAGE) has been identified as a susceptibility gene for chronic obstructive pulmonary disease (COPD) in genome-wide association studies (GWASs). However, less is known about how RAGE is involved in the pathogenesis of COPD. To determine the molecular mechanism by which RAGE influences COPD in experimental COPD models, we investigated the efficacy of the RAGE-specific antagonist FPS-ZM1 administration in and COPD models. We injected elastase intratracheally and the RAGE antagonist FPS-ZM1 in mice, and the infiltrated inflammatory cells and cytokines were assessed by ELISA. Cellular expression of RAGE was determined in protein, serum, and bronchoalveolar lavage fluid of mice and lungs and serum of human donors and patients with COPD. Downstream damage-associated molecular pattern (DAMP) pathway activation and and in patients with COPD was assessed by immunofluorescence staining, Western blot analysis, and ELISA. The expression of membrane RAGE in initiating the inflammatory response and of soluble RAGE acting as a decoy were associated with up-regulation of the DAMP-related signaling pathway Nrf2. FPS-ZM1 administration significantly reversed emphysema in the lung of mice. Moreover, FPS-ZM1 treatment significantly reduced lung inflammation in , but not in mice. Thus, our data indicate for the first time that RAGE inhibition has an essential protective role in COPD. Our observation of RAGE inhibition provided novel insight into its potential as a therapeutic target in emphysema/COPD.-Lee, H., Park, J.-R., Kim, W. J., Sundar, I. K., Rahman, I., Park, S.-M., Yang. S.-R. Blockade of RAGE ameliorates elastase-induced emphysema development and progression RAGE-DAMP signaling.

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“…Cigarette smoke (CS) is a major risk factor for the development of COPD, which leads to airway inflammation associated with neutrophils and macrophages in the airway [2021]. These cells produced pro-inflammatory cytokines, chemokines, and proteases exhibiting aggravation of airway inflammation, mucus secretion, and structural alteration [22].…”

Section: Discussionmentioning

confidence: 99%

HemoHIM, a herbal preparation, alleviates airway inflammation caused by cigarette smoke and lipopolysaccharide

Shin

Kim

et al. 2017

Lab Anim Res

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HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-α, interleukin (IL)-6 and IL-1β in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

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Cigarette smoke-mediated oxidative stress induces apoptosis via the MAPKs/STAT1 pathway in mouse lung fibroblasts

Cited by 55 publications

References 47 publications

Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Blockade of RAGE ameliorates elastase‐induced emphysema development and progression via RAGE‐DAMP signaling

HemoHIM, a herbal preparation, alleviates airway inflammation caused by cigarette smoke and lipopolysaccharide

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