Yun Sun's research while affiliated with Peking University Third Hospital and other places
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Publications (7)
Epithelial mesenchymal transition (EMT) is a contributing factor in remodeling events of chronic obstructive pulmonary disease (COPD). Hydrogen sulfide (H2S) has been implicated in the pathogenesis of COPD, but the effect of H2S in regulating EMT and the underlying mechanisms is not clear. In this study, we assessed endoplasmic reticulum (ER) stres...
Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide, which is usually caused by exposure to noxious particles or gases. Hydrogen sulfide (H2S), as an endogenous gasotransmitter, is involved in the pathogenesis of COPD, but its role in COPD is little known. To investigate the role of H2S in COPD, a rat model of COPD wa...
Background: Apoptosis of lung structural cells contributes to the process of lung damage and remodeling in chronic obstructive pulmonary disease (COPD). Our previous studies demonstrated that exogenous hydrogen sulfide (H2S) can reduce the lung tissue pathology score, anti-inflammation and anti-oxidation effects in COPD, but the effect of H2S in re...
Oxidative stress and inflammation play crucial role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Most patients with COPD show a poor response to corticosteroids. Hydrogen sulfide (H2S ) has been implicated in the pathogenesis of COPD, but its expression and effects in lung tissue from COPD patients are not clear. In peripher...
Objective:
To explore the effects of hydrogen sulfide on nicotine-induced bronchial epithelial cell endoplasmic reticulum (ER) stress and apoptosis.
Methods:
Nicotine was used to establish the apoptotic model in human bronchial epithelial cell line (16HBE) for mimicing the effect of cigarette smoke on apoptosis. The 16HBE cells were grouped by t...
Objective:
To explore the role of cortistatin (CST) in rats with chronic obstructive pulmonary disease (COPD).
Methods:
A total of 16 healthy male Sprague-Dawley rats were randomly divided into control and COPD model groups (n=8 each). The COPD model group received an inhalation of passive smoking while the control group was treated normally. Af...
Exhaled nitric oxide (NO) is a noninvasive biomarker of airway inflammation in pulmonary diseases. Hydrogen sulfide (H2S), as the third member of the gasotransmitter family, is involved in the pathophysiological process in lung diseases. H2S also exists in exhaled breath and can be sampled non-invasively. The study investigated the level of exhaled...
Citations
... In addition to modulating the NLRP3 inflammasome, IRE1α can promote CS-induced airway inflammation by activating the NF-κB signaling pathway [129,130]. Furthermore, the activation of IRE1α played a crucial role in the nicotine-induced epithelialmesenchymal transition and decreased cell migration capacity in human bronchial epithelial cells [152]. Epithelial-mesenchymal transition is a pivotal contributor to airway remodeling in COPD. . ...
... We do not investigate the effect of arecoline on the activity of CBS and 3-MST in PC12 cells and this part is for further to inverstigate. It is worth noting that H 2 S has a beneficial effectcan by inhibiting ER stress in multiple disease [45,46], which point out that the effect of H 2 S on ER stress may also contribute to arecoline-exhibited neurotoxicity. ...
... These reactions preserve intracellular homeostasis by facilitating correct protein folding, destroying fold-deficient proteins, and weakening protein translation processes [5]. Apoptosis is induced if stress persists unresolved and damage is not repaired after an initial protective phase [8,36]. Our results demonstrated that CS exposure induced ultrastructural changes in the ER morphology of lung tissue. ...
... CGL mRNA, protein, and enzyme activities in select mammalian tissues[29][30][31][32][33][34] [35, 36] [37] [38, 39] [40] [29, 30, 41-43] [29][29,[44][45][46][47][48][49][50][51][52][53] [29,31,43,48,[54][55][56][57][58][59][60][61][62][63] [29,61] [29] ...
... Exhaled sulfide was lower in COPD patients compared to healthy subjects and correlated with airway obstruction in another study [193]. Other authors found that exhaled H 2 S was correlated with FeNO but not with sputum inflammatory cells in COPD [194]. Furthermore, it was found that air pollution causes an increase in exhaled H 2 S concentration in patients with COPD, likely due to worsening airway inflammation [195]. ...
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