scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

scholarly journals Protective Effects of Licochalcone A Improve Airway Hyper-Responsiveness and Oxidative Stress in a Mouse Model of Asthma

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 617 ◽  
Author(s):  
Wen-Chung Huang ◽  
Chien-Yu Liu ◽  
Szu-Chuan Shen ◽  
Li-Chen Chen ◽  
Kuo-Wei Yeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Therapeutic Potential ◽  
Intercellular Adhesion Molecule ◽  
Eosinophil Infiltration ◽  
Licochalcone A ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
Oxidative Responses

Licochalcone A was isolated from Glycyrrhiza uralensis and previously reported to have antitumor and anti-inflammatory effects. Licochalcone A has also been found to inhibit the levels of Th2-associated cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. However, the molecular mechanism underlying airway inflammation and how licochalcone A regulates oxidative stress in asthmatic mice are elusive. In this study, we investigated whether licochalcone A could attenuate inflammatory and oxidative responses in tracheal epithelial cells, and whether it could ameliorate oxidative stress and airway inflammation in asthmatic mice. Inflammatory human tracheal epithelial (BEAS-2B) cells were treated with licochalcone A to evaluate oxidative responses and inflammatory cytokine levels. In addition, BALB/c mice were sensitized with ovalbumin (OVA) and injected intraperitoneally with licochalcone A (5 or 10 mg/kg). Licochalcone A significantly inhibited reactive oxygen species, eotaxin, and proinflammatory cytokines in BEAS-2B cells. Licochalcone A also decreased intercellular adhesion molecule 1 levels in inflammatory BEAS-2B cells, blocking monocyte cell adherence. We also found that licochalcone A significantly decreased oxidative responses, reduced malondialdehyde levels, and increased glutathione levels in the lungs of OVA-sensitized mice. Furthermore, licochalcone A decreased airway hyper-responsiveness, eosinophil infiltration, and Th2 cytokine production in the BALF. These findings suggest that licochalcone A alleviates oxidative stress, inflammation, and pathological changes by inhibiting Th2-associated cytokines in asthmatic mice and human tracheal epithelial cells. Thus, licochalcone A demonstrated therapeutic potential for improving asthma.

scholarly journals Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 295 ◽  
Author(s):  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Ming-Chin Yu ◽  
Kuo-Wei Yeh ◽  
Szu-Chuan Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Lavage Fluid ◽  
Eosinophil Infiltration ◽  
Sesame Seeds ◽  
Cytokine Levels ◽  
And Oxidative Stress

Sesamol, isolated from sesame seeds (Sesamum indicum), was previously shown to have antioxidative, anti-inflammatory, and anti-tumor effects. Sesamol also inhibited lipopolysaccharide (LPS)-induced pulmonary inflammatory response in rats. However, it remains unclear how sesamol regulates airway inflammation and oxidative stress in asthmatic mice. This study aimed to investigate the efficacy of sesamol on oxidative stress and airway inflammation in asthmatic mice and tracheal epithelial cells. BALB/c mice were sensitized with ovalbumin, and received oral sesamol on days 14 to 27. Furthermore, BEAS-2B human bronchial epithelial cells were treated with sesamol to investigate inflammatory cytokine levels and oxidative responses in vitro. Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung, airway hyperresponsiveness, and T helper 2 cell-associated (Th2) cytokine expressions in bronchoalveolar lavage fluid and the lungs. Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice. We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells. Moreover, sesamol alleviated reactive oxygen species formation, and suppressed intercellular cell adhesion molecule-1 (ICAM-1) expression, which reduced monocyte cell adherence. We demonstrated that sesamol showed potential as a therapeutic agent for improving asthma.

scholarly journals Helminthostachys zeylanica Water Extract Ameliorates Airway Hyperresponsiveness and Eosinophil Infiltration by Reducing Oxidative Stress and Th2 Cytokine Production in a Mouse Asthma Model

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Wen-Chung Huang ◽  
Nai-Chun Ting ◽  
Yu-Ling Huang ◽  
Li-Chen Chen ◽  
Chwan-Fwu Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Airway Hyperresponsiveness ◽  
Cytokine Production ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Th2 Cytokine ◽  
Tracheal Epithelial ◽  
Helminthostachys Zeylanica

Helminthostachys zeylanica is a traditional folk herb used to improve inflammation and fever in Taiwan. Previous studies showed that H. zeylanica extract could ameliorate lipopolysaccharide-induced acute lung injury in mice. The aim of this study was to investigate whether H. zeylanica water (HZW) and ethyl acetate (HZE) extracts suppressed eosinophil infiltration and airway hyperresponsiveness (AHR) in asthmatic mice, and decreased the inflammatory response and oxidative stress in tracheal epithelial cells. Human tracheal epithelial cells (BEAS-2B cells) were pretreated with various doses of HZW or HZE (1 μg/ml–10 μg/ml), and cell inflammatory responses were induced with IL-4/TNF-α. In addition, female BALB/c mice sensitized with ovalbumin (OVA), to induce asthma, were orally administered with HZW or HZE. The result demonstrated that HZW significantly inhibited the levels of proinflammatory cytokines, chemokines, and reactive oxygen species in activated BEAS-2B cells. HZW also decreased ICAM-1 expression and blocked monocytic cells from adhering to inflammatory BEAS-2B cells in vitro. Surprisingly, HZW was more effective than HZE in suppressing the inflammatory response in BEAS-2B cells. Our results demonstrated that HZW significantly decreased AHR and eosinophil infiltration, and reduced goblet cell hyperplasia in the lungs of asthmatic mice. HZW also inhibited oxidative stress and reduced the levels of Th2 cytokines in bronchoalveolar lavage fluid. Our findings suggest that HZW attenuated the pathological changes and inflammatory response of asthma by suppressing Th2 cytokine production in OVA-sensitized asthmatic mice.

scholarly journals Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4210
Author(s):  
Yan Zhou ◽  
Chunxiu Zhou ◽  
Xutao Zhang ◽  
Chi Teng Vong ◽  
Yitao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Vascular Function ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Ex Vivo ◽  
Diabetic Mice ◽  
And Oxidative Stress

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

Application of glutathione to antagonize H2O2-induced oxidative stress in rat tracheal epithelial cells

2016 ◽  
Vol 11 (1) ◽  
pp. 59-63
Author(s):  
Jian Zou ◽  
Jinbo Yu ◽  
Yuqing Zhu ◽  
Jiali Zhu ◽  
Jing Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

scholarly journals Levofloxacin Inhibits Rhinovirus Infection in Primary Cultures of Human Tracheal Epithelial Cells

2012 ◽  
Vol 56 (8) ◽  
pp. 4052-4061 ◽  
Author(s):  
Mutsuo Yamaya ◽  
Hidekazu Nishimura ◽  
Yukimasa Hatachi ◽  
Hiroyasu Yasuda ◽  
Xue Deng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Bacterial Infections ◽  
Mrna Level ◽  
Primary Cultures ◽  
Intercellular Adhesion Molecule ◽  
Soluble Form ◽  
Chronic Obstructive ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

ABSTRACTRespiratory virus infections, including infections with rhinoviruses (RVs), are related to exacerbations of chronic obstructive pulmonary disease (COPD). A new quinolone antibiotic, levofloxacin (LVFX), has been used to treat bacterial infections that cause COPD exacerbations as well as bacterial infections that are secondary to viral infection in COPD patients. However, the inhibitory effects of LVFX on RV infection and RV infection-induced airway inflammation have not been studied. We examined the effects of LVFX on type 14 rhinovirus (RV14) (a major human RV) infection of human tracheal epithelial cells pretreated with LVFX. LVFX pretreatment reduced the RV14 titer, the level of cytokines in the supernatant, the amount of RV14 RNA in the cells after RV14 infection, and the cells' susceptibility to RV14 infection. LVFX pretreatment decreased the mRNA level of intercellular adhesion molecule 1 (ICAM-1), a receptor for RV14, in the cells and the concentration of the soluble form of ICAM-1 in the supernatant before RV14 infection. LVFX pretreatment also decreased the number and the fluorescence intensity of the acidic endosomes from which RV14 RNA enters the cytoplasm. LVFX pretreatment inhibited the activation of nuclear factor κB proteins, including p50 and p65, in nuclear extracts. LVFX pretreatment did not reduce the titers of RV2 (a minor human RV) but reduced the titers of RV15 (a major human RV). These results suggest that LVFX inhibits major-group rhinovirus infections in part by reducing ICAM-1 expression levels and the number of acidic endosomes. LVFX may also modulate airway inflammation in rhinoviral infections.

Sequoyitol Alleviates High Glucose-Induced Inflammation, Oxidative Stress and Apoptosis of Retina Epithelial Cells

2021 ◽  
Vol 11 (5) ◽  
pp. 1003-1009
Author(s):  
Liping Hu ◽  
Rui Zhang ◽  
Jianhua Wu ◽  
Chao Feng ◽  
Li Kong
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Cell Viability ◽  
Inflammatory Cytokines ◽  
High Glucose ◽  
Cell Apoptosis ◽  
Therapeutic Potential ◽  
Promoting Effect ◽  
Related Factors ◽  
And Oxidative Stress

Diabetic retinopathy (DR) is a serious microvascular complication of diabetes, contributing to visual impairment and blindness. Sequoyitol (Seq), a form of inositol derivatives, has been demonstrated to be a therapeutic potential for diabetes and diabetic nephropathy. The aim of this study is to explore the effects of Seq on DR. ARPE-19 cells were cultured in high glucose (HG) condition to simulate DR in vitro. Seq (1,10 and 20 µM) was applied for treatment. CCK-8 assay was performed to detect cell viability. Flow cytometry analysis was conducted to determine cell apoptosis rate. The production level of inflammatory cytokines and oxidative stress-related factors were determined using their commercial kits. The protein expressions of corresponding genes were detected using western blotting. The results revealed that Seq significantly increased cell viability and protein expression of PCNA and Ki67 which were decreased after HG induction. HG promoted cell apoptosis by decreasing protein expression of Bcl-2 and increasing protein expression of Bax and cleaved caspase-3, which was then reversed by Seq treatment. Besides, Seq abolished the promoting effects of HG on the production of pro-inflammatory cytokines and oxidative stress-related factors. Furthermore, Seq suppressed the promoting effect of HG on the activation of NF-κB signaling by inhibiting phosphorylation of kBa and NF-κB nucleus translocation. These results indicated that Seq might protect ARPE-19 cells against HG-induced cell viability, apoptosis, inflammation and oxidative stress by regulating NF-κB signaling, providing evidence for the potential application of Seq in the therapy of DR.

scholarly journals Coenzyme Q10 attenuates airway inflammation and oxidative stress in neonatal asthmatic rats

2020 ◽  
Vol 19 (9) ◽  
pp. 1969-1975
Author(s):  
Jingwei Peng ◽  
Jilong Ma ◽  
Lan Zhang ◽  
Banghao Lu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Airway Inflammation ◽  
Coenzyme Q10 ◽  
Therapeutic Potential ◽  
Inflammatory Cells ◽  
Th2 Cytokines ◽  
Gene Expressions ◽  
Keywords Asthma ◽  
And Oxidative Stress

Purpose: To determine the therapeutic effect of coenzyme Q10 (CoQ10) on ovalbumin (OVA)-provoked asthma in neonatal rats.Methods: Asthma was induced by exposing neonatal rats to OVA. The levels of SOD, CAT, GPx, GSH, MDA and MPO were estimated using standard biochemical kits, while ELISA was used to measure the concentrations of Ig E and Th2 cytokines. Gene expressions were assayed with qRT-PCR, and protein expressions were determined with western blotting.Results: OVA treatment led to increases in levels of BALF inflammatory cells, lipid peroxidation, serum IgE and BALF Th2 cytokines, but it decreased antioxidant levels. Furthermore, the protein expression of NF-κB and mRNA expression levels of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) were upregulated in the asthmatic rats (p < 0.05). However, coenzyme Q10 supplementation significantly decreased lipid peroxidation, and reduced inflammatory cells and IgE levels, while the antioxidant levels were enhanced (p < 0.05). Moreover, coenzyme Q10 reduced the levels of Th2 cytokines and downregulated the expressions of NF-κB, TNF-α, IL-6, and iNOS in the neonatal asthmatic rats (p < 0.05).Conclusion: Coenzyme Q10 attenuates airway inflammation and oxidative stress in neonatal asthmatic rats. Thus, coenzyme Q10 has promising therapeutic potential in the management of asthma. Keywords: Asthma, Neonatal, Coenzyme Q10, Th2, cytokines, Oxidative stress, Antiinflammation

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