Effect of fudosteine, a cysteine derivative, on airway hyperresponsiveness, inflammation, and remodeling in a murine model of asthma

Ueno-Iio, Tomoe; Shibakura, Misako; Iio, Koji; Tanimoto, Yasushi; Kanehiro, Arihiko; Tanimoto, Mitsune; Kataoka, Masao

doi:10.1016/j.lfs.2013.03.022

Cited by 11 publications

(4 citation statements)

References 36 publications

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“…MMP-2 and MMP-9 belong to a family of extracellular proteases that are responsible for the degradation of the extracellular matrix during tissue and vascular remodeling [18, 27]. Levels of MMP-2, MMP-9, and TIMP-1 are significantly increased in BALF from patients and animals with allergic asthma [28–30]. Felsen et al found that MMP-2 and MMP-9 are up-regulated in the lungs of OVA-challenged mice and the highest MMP-2 and MMP-9 activity was detected in the areas of inflammation surrounding the airways, a major site of tissue remodeling [31].…”

Section: Discussionmentioning

confidence: 99%

CTGF upregulation correlates with MMP-9 level in airway remodeling in a murine model of asthma

Lin¹,

Chou²,

Chiang³

et al. 2017

aoms

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IntroductionConnective tissue growth factor (CTGF) mediates hypertrophy, proliferation, and extracellular matrix synthesis. Matrix metalloproteinase (MMP) plays a role in airway extracellular matrix remodeling. The correlation between CTGF and MMP in airway remodeling of asthma was unknown. This study investigated lung CTGF expression and its correlation with MMP and airway structural changes in a murine model of asthma.Material and methodsFemale BALB/c mice were sensitized and challenged by intraperitoneal injections and intranasal phosphate-buffered saline (PBS) or ovalbumin (OVA). Airway responsiveness and serum OVA-specific IgE were measured. Airway structural changes were quantified by morphometric analysis. Differential cell counts and MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 were evaluated in bronchoalveolar lavage fluid (BALF). Lung CTGF was determined by Western blot.ResultsSerum OVA-specific IgE level and airway responsiveness in enhanced pause (Penh) is significantly higher in sensitized mice challenged with OVA compared to PBS-challenged mice. MMP-2, MMP-9, and TIMP-1 in BALF were significantly higher in OVA mice. Airway structural changes of animals’ lungs with OVA challenge showed increased thickness of the smooth muscle layer and numbers of Goblet cells and inflammatory cells and eosinophils near airways and perivascular areas. Lung CTGF expression significantly increased in OVA-challenged mice. CTGF expressions positively correlated with MMP-9 (r = 0.677, p < 0.05), TIMP-1 (r = 0.574, p < 0.05) and thickness of the smooth muscle layer (r = 0.499, p < 0.05).ConclusionsThis study indicates that CTGF upregulation correlates with MMP-9, probably involved in the pathogenesis of airway remodeling of asthma.

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Section: Discussionmentioning

confidence: 99%

CTGF upregulation correlates with MMP-9 level in airway remodeling in a murine model of asthma

Lin¹,

Chou²,

Chiang³

et al. 2017

aoms

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“…Through the manufacture and release of proinflammatory mediators, Eos can amplify the expression of Th1, Th2, and Th17 cytokines and chemokines suggesting that they play a vital role in the adaptive immune responses [41]. Activated Eos can secrete some basic proteins which may also be associated with the pathophysiology of asthma such as MBP, ECP, and EPO [8]. Previous studies have demonstrated that MBP can increase vascular permeability, bronchoconstriction, and airway epithelial damage; then remodeling is associated with more severe airflow obstruction, and AHR made in asthma.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies indicate that asthma is a chronic inflammatory airway disease that is caused by a variety of cells like eosinophils (Eos), mast cells, neutrophils, T lymphocytes, airway epithelial cells, and a number of cytokines [7]. These cells secrete several chemical mediators, such as major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPO), lipid ecosystems, elastase, and Th2 cytokines, such as IL-4 (a switch factor for IgE synthesis), IL-5, and IL-13 [8]. Therefore, these cells are considered as major targets for basic and therapeutic research.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of Sihuangxiechai Decoction on Ovalbumin‐Induced Airway Inflammation in Guinea Pigs

Huang

Tao

Feng

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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The aim of this study was to investigate the effect of sihuangxiechai decoction on asthmatic Guinea pig model which was sensitized by intraperitoneal (i.p.) injection of ovalbumin (OVA) and challenged by OVA inhalation to induce chronic airway inflammation. Differential cell counts of cytospins were performed after staining with Giemsa solution. The quantity of leukocytes and its classification in bronchoalveolar lavage fluid (BALF) and blood were evaluated by blood cell analyzer and microscope. Histological analysis of the lung was performed by hematoxylin and eosin (H&E) staining. The levels of interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-α) in BALF and serum were detected by radioimmunoassay (RIA). The total number of leukocytes in BALF and blood has no significant difference between Sihuangxiechaitang decoction treated group and dexamethasone (DXM) treated group but was significantly lower than those of asthma group. The percentage of eosinophils in lung tissues of sihuangxiechai decoction treated group was significantly lower than that of asthma group. The results demonstrated that the levels of IL-4 and TNF-α in the sihuangxiechai decoction treated group were significantly reduced compared with the asthma group. In conclusion, these findings demonstrate that sihuangxiechai decoction has a protective effect on OVA-induced asthma in reducing airway inflammation and airway hyperresponsiveness (AHR) in a Guinea pig model and may be useful as an adjuvant therapy for the treatment of bronchial asthma.

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“…It works as a mucoactive agent by inhibiting MUC5AC gene expression and related signaling pathways. 66 , 67 Fudosteine has been shown to inhibit peroxynitrite-induced airway nitrosative stress in lung epithelial cells by direct scavenging of peroxynitrite and plays a protective role in COPD. 68 These findings suggest that fudosteine may be useful for controlling oxidative/carbonyl stress-related mucus secretion in patients with asthma, bronchiectasis, or COPD.…”

Section: Treatment Of Airway Mucus Hypersecretionmentioning

confidence: 99%

Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition)

Shen¹,

Huang²,

Kang³

et al. 2018

COPD

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Airway mucus hypersecretion is one of the most important characteristics of chronic airway inflammatory diseases. Evaluating and managing airway mucus hypersecretion is of great importance for patients with chronic airway inflammatory diseases. This consensus statement describes the pathogenesis, clinical features, and the management of airway mucus hypersecretion in patients with chronic airway inflammatory diseases in the People’s Republic of China. The statement has been written particularly for respiratory researchers, pulmonary physicians, and patients.

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Effect of fudosteine, a cysteine derivative, on airway hyperresponsiveness, inflammation, and remodeling in a murine model of asthma

Cited by 11 publications

References 36 publications

CTGF upregulation correlates with MMP-9 level in airway remodeling in a murine model of asthma

CTGF upregulation correlates with MMP-9 level in airway remodeling in a murine model of asthma

Inhibitory Effect of Sihuangxiechai Decoction on Ovalbumin‐Induced Airway Inflammation in Guinea Pigs

Management of airway mucus hypersecretion in chronic airway inflammatory disease: Chinese expert consensus (English edition)

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