Hydrogen coadministration slows the development of COPD-like lung disease in a cigarette smoke-induced rat model

Liu, Xiaoyu; Ma, Cuiqing; Wang, Xiaoyu; Wang, Wenjing; Zhu, Liu; Wang, Xiansheng; Wang, Pengyu; Sun, Wenjing; Xue, Baojian

doi:10.2147/copd.s124547

Cited by 35 publications

(28 citation statements)

References 40 publications

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“…Therefore, how to improve the bronchial mucosal immunity is a core issue. Our previous study showed that hydrogen inhalation could visibly reduce inflammation and apoptosis, and improve cardiovascular function, suggesting a "significant effect" of hydrogen inhalation on COPD (21). Our results provided new information that treatment with hydrogen could ameliorate pathological changes, airway remodeling as well as SIgA expression.…”

Section: Discussionsupporting

confidence: 57%

“…In recent years, a number of studies have shown that hydrogen therapy has a positive effect on various diseases (17)(18)(19)(20). Liu et al in our team found that different concentrations of hydrogen inhalation could significantly reduce inflammation and apoptosis, protect mitochondria, and ameliorate cardiovascular function in COPD rat model (21). A key question is whether there exist a possibility that hydrogen inhalation will have a positive effect on SIgA expression in rat model of COPD , which is to be tested in the experiment.…”

Section: Introductionmentioning

confidence: 97%

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Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

Sun

Zhu

et al. 2020

Preprint

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AbstractBackgroundRecently, some researchers have reported that PIgR expression is down-regulated in Chronic Obstructive Pulmonary Disease (COPD) and SIgA deficiency correlates with severity of airflow obstruction. What’ s more, some studies have demonstrated that 2 percent of hydrogen or hydrogen water is effective in treating and preventing various diseases.ObjectivesThe aim of this study was to observe the effect of hydrogen on the expression of SIgA, PIgR, IL-4, IL-5, TGF-β1 and IL-40 in lung tissue of COPD rats, to study the relationship between lung pathology parameter and SIgA, PIgR, therefore we can understand the effect of hydrogen on the development of COPD by changing SIgA expression of airway mucosal in COPD rats.MethodsA rat model of COPD was established by cigarette smoke exposure, and different concentrations of hydrogen were inhaled as intervention measures. After 4 months of cigarette smoke exposure, pathologic changes and airway wall remodeling of the lung were assessed by optical microscope. The protein expressions of SIgA, PIgR, IL-4, IL-5, TGF-β1 as well as IL-40 in the lung tissues were observed by immunohistochemistry or Western blot. The correlation between lung pathology parameter and the expression of SIgA, PIgR was analyzed. The correlation between SIgA and the expression of IL-4, IL-5, TGF-β1 and IL-40 was analyzed.ResultsThe results showed that hydrogen inhalation significantly ameliorated lung pathology and airway wall remodeling, increased the protein expression of SIgA, PIgR, IL-4, IL-5, and IL-40, and reduced the protein expression of TGF-β1.ConclusionsInhalation of 22% and 41.6% hydrogen showed a better effect than inhalation of 2% hydrogen. Hydrogen inhalation can significantly improve the expression of SIgA on the mucosal surface of COPD rats, which may be one of the mechanisms which hydrogen works on COPD pathogenesis.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 97%

Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

Sun

Zhu

et al. 2020

Preprint

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“…Moreover, H 2 can be produced conveniently (e.g., in an ambulance) and inexpensively by electrolyzing water. H 2 generator is a novel equipment and has reportedly been used in renal calcium oxalate deposition [9], cerebral ischemia-reperfusion injury [10], liver ischemia-reperfusion injury [11], chronic obstructive pulmonary disease model rats [12], and sanitation workers exposed to haze [13], with promising outcomes in alleviating inflammation and biological safety. However, data on clinical use of H 2 in patients with tracheal stenosis remain so far insufficient.…”

Section: Introductionmentioning

confidence: 99%

Breathing Hydrogen-Oxygen Mixture Decreases Inspiratory Effort in Patients with Tracheal Stenosis

Zhou

Zhong

et al. 2018

Respiration

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Background: Hydrogen-oxygen mixture (H₂-O₂) may reduce airway resistance in patients with acute severe tracheal stenosis, yet data supporting the clinical use of H₂-O₂ are insufficient. Objectives: To evaluate the efficacy and safety of breathing H₂-O₂ in acute severe tracheal stenosis. Methods: Thirty-five consecutive patients with severe acute tracheal stenosis were recruited in this prospective self-control study. Air, H₂-O₂ and O₂ inhalation was given in 4 consecutive breathing steps: air for 15 min, H₂-O₂ (6 L per min, H₂:O₂ = 2: 1) for 15 min, oxygen (3 L per min) for 15 min, and H₂-O₂ for 120 min. The primary endpoint was inspiratory effort as assessed by diaphragm electromyography (EMGdi); the secondary endpoints were transdiaphragmatic pressure (Pdi), Borg score, vital signs, and impulse oscillometry (IOS). The concentration of H₂ in the ambient environment was obtained with 12 monitors. Adverse reactions during the inhalation were recorded. Results: The mean reduction in the EMGdi under H₂-O₂ was 10.53 ± 6.83%. The EMGdi significantly decreased during 2 H₂-O₂ inhalation steps (Steps 2 and 4) compared with air (Step 1) and O₂ (Step 3) (52.95 ± 15.00 vs. 42.46 ± 13.90 vs. 53.20 ± 14.74 vs. 42.50 ± 14.12% for Steps 1 through 4, p < 0.05). The mean reduction in the Pdi under H₂-O₂ was 4.77 ± 3.51 cmH₂O. Breathing H₂-O₂ significantly improved the Borg score and resistance parameters of IOS but not vital signs. No adverse reactions occurred. H₂ was undetectable in the environment throughout the procedure. Conclusions: Breathing H₂-O₂ may reduce the inspiratory effort in patients with acute severe tracheal stenosis and can be used for this purpose safely.

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“…; Liu et al. ). Though, these studies did not include an in‐depth look into the different membrane structures.…”

Section: Discussionmentioning

confidence: 98%

Endoplasmic reticulum, Golgi, and lysosomes are disorganized in lung fibroblasts from chronic obstructive pulmonary disease patients

et al. 2018

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Chronic Obstructive Pulmonary Disease (COPD) is often caused by smoking and other stressors. This causes oxidative stress, which induces numerous changes on both the transcriptome and proteome of the cell. We aimed to examine if the endomembrane pathway, including the endoplasmic reticulum (ER), Golgi, and lysosomes, was disrupted in fibroblasts from COPD patients as opposed to healthy ever‐smokers or never‐smokers, and if the response to stress differed. Different cellular compartments involved in the endomembrane pathway, as well as mRNA expression and apoptosis, were examined before and after the addition of stress in lung fibroblasts from never‐smokers, ever‐smokers, and patients with COPD. We found that the ER, Golgi, and lysosomes were disorganized in fibroblasts from COPD patients under baseline conditions. After a time course with ER stress inducing chemicals, changes to the phenotypes of cellular compartments in COPD patient fibroblasts were observed, and the expression of the ER stress‐induced gene ERP72 was upregulated more in the COPD patient's cells compared to ever‐smokers or never‐smokers. Lastly, a tendency of increased active Caspase‐3 was observed in COPD fibroblasts. Our results show that COPD patients have phenotypic changes in the lung fibroblasts endomembrane pathway, and respond differently to stress. Furthermore, these fibroblasts were cultured for several weeks outside the body, but they were not able to regain proper ER structure, indicating that the internal changes to the endomembrane system are permanent in smokers. This vulnerability to cellular stress might be a cause as to why some smokers develop COPD.

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Hydrogen coadministration slows the development of COPD-like lung disease in a cigarette smoke-induced rat model

Cited by 35 publications

References 40 publications

Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

Breathing Hydrogen-Oxygen Mixture Decreases Inspiratory Effort in Patients with Tracheal Stenosis

Endoplasmic reticulum, Golgi, and lysosomes are disorganized in lung fibroblasts from chronic obstructive pulmonary disease patients

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