Electroacupuncture Reduces Hypothalamic and Medullary Expression of Orexins and their Receptors in a Rat Model of Chronic Obstructive Pulmonary Disease

2018 ◽  
Vol 36 (5) ◽  
pp. 312-318 ◽  
Author(s):  
Xin-Fang Zhang ◽  
Qin Qin ◽  
Wen-Ye Geng ◽  
Chuan-Wei Jiang ◽  
Yong Liu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Protein Expression ◽  
Pulmonary Function ◽  
Pulmonary Disease ◽  
Rat Model ◽  
Normal Group ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Objectives Decreased lung function in chronic obstructive pulmonary disease (COPD) is correlated with abnormal excitability of the respiratory centre where orexin neuropeptides from the hypothalamus are responsible for regulating respiration. We hypothesised that improvements in pulmonary function with electroacupuncture (EA) may be related to orexins in a rat model of COPD. Methods The COPD model was established by cigarette smoke exposure and lipopolysaccharide injection. Modelled rats received EA at BL13 and ST36 for two weeks, after which lung function was tested. Orexin levels in the hypothalamus and medulla were detected by ELISA, while mRNA/protein expression and localisation of orexins and their receptors were investigated using real time PCR, Western blotting and immunohistochemistry, respectively. Results The decrease in lung function observed in COPD rats was improved after EA treatment. Orexin levels in the hypothalamus and medulla were significantly higher in COPD rats than in normal rats, but were significantly reduced in the EA-treated group. There was a negative correlation between orexin content and lung function. In the hypothalamus, mRNA and protein expression and immunoreactivity of orexins were significantly higher in the COPD group than in the normal group, but a significant decrease was observed after EA. In the medulla, the expression and immunoreactivity of orexin receptors were significantly higher in the COPD group than in the normal group, but a significant decrease was observed after EA. Conclusions The positive effect of EA on pulmonary function in COPD rats may be related to downregulation of orexins and their receptors in the medulla.

scholarly journals Computed tomography-derived area and density of pectoralis muscle associated disease severity and longitudinal changes in chronic obstructive pulmonary disease: a case control study

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
So Hyeon Bak ◽  
Sung Ok Kwon ◽  
Seon-Sook Han ◽  
Woo Jin Kim
Keyword(s):  
Computed Tomography ◽  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Function ◽  
Pulmonary Disease ◽  
Disease Severity ◽  
Chronic Obstructive ◽  
Pectoralis Muscle ◽  
Obstructive Pulmonary Disease ◽  
Longitudinal Changes

Abstract Background Muscle wasting is associated with prognosis in patients with chronic obstructive pulmonary disease (COPD). The cross-sectional area of skeletal muscles on computed tomography (CT) could serve as a method to evaluate body composition. The present study aimed to determine the ability of CT-derived pectoralis muscle area (PMA) and pectoralis muscle density (PMD) to determine the severity of COPD and change in longitudinal pulmonary function in patients with COPD. Methods A total of 293 participants were enrolled in this study, a whom 222 had undergone at least two spirometry measurements within 3 years after baseline data acquisition. PMA and PMD were measured from a single axial slice of chest CT above the aortic arch at baseline. The emphysema index and bronchial wall thickness were quantitatively assessed in all scans. The generalized linear model was used to determine the correlation between PMA and PMD measurements and pulmonary function. Results PMA and PMD were significantly associated with baseline lung function and the severity of emphysema (P < 0.05). Patients with the lowest PMA and PMD exhibited significantly more severe airflow obstruction (β = − 0.06; 95% confidence interval: − 0.09 to − 0.03]. PMA was statistically associated with COPD assessment test (CAT) score (P = 0.033). However, PMD did not exhibit statistically significant correlation with either CAT scores or modified Medical Research Council scores (P > 0.05). Furthermore, neither PMA nor PMD were associated with changes in forced expiratory volume in 1 s over a 3-year periods. Conclusions CT-derived features of the pectoralis muscle may be helpful in predicting disease severity in patients with COPD, but are not necessarily associated with longitudinal changes in lung function.

scholarly journals Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of SIRT1 in a rat model

2019 ◽  
Vol 47 (10) ◽  
pp. 4764-4774 ◽  
Author(s):  
Feng Tang ◽  
Chunhua Ling
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protein Expression ◽  
Pulmonary Disease ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
High Dose ◽  
Obstructive Pulmonary Disease ◽  
Gene And Protein Expression

Objectives The ability of curcumin to activate SIRT1 and thereby promote autophagy and inhibit endoplasmic reticulum stress (ERS) in chronic obstructive pulmonary disease (COPD) remains unclear. We investigated the relationship between curcumin and SIRT1 activation in relation to autophagy and ERS in COPD. Methods We developed a rat COPD model by cigarette smoke exposure, and divided the rats into control, COPD, COPD + low-dose curcumin (50 mg/kg), COPD + medium-dose curcumin (100 mg/kg), COPD + high-dose curcumin (150 mg/kg), and COPD + high-dose curcumin + sirtinol (2 mM, 30 μL/kg) groups. Apoptosis was detected by TUNEL assay. SIRT1 gene and protein expression, and protein expression of autophagy-related genes LC3-I, LC3-II, and Beclin1, and ERS-related genes CHOP and GRP78 were measured by reverse transcription-polymerase chain reaction and western blot. Results SIRT1, LC3-I, LC3-II, and Beclin1 expression were significantly decreased and CHOP and GRP78 were enhanced in COPD compared with control rats. Curcumin increased the expression of SIRT1, LC3-I, LC3-II, and Beclin1 and decreased the expression of CHOP and GRP78 in COPD rats. The alleviating effects of curcumin on COPD in the SIRT1-inhibition group were reversed by suppressing LC3-I, LC3-II, and Beclin1 and increasing CHOP and GRP78. Conclusion Curcumin might alleviate COPD by promoting autophagy and inhibiting ERS through SIRT1 activation.

scholarly journals Ability of γ-tocotrienol to Mitigate Inflammation and Preserve Lung Function in a Model of E-Cigarette Induced Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 437-437
Author(s):  
Maureen Meister ◽  
Will Conrad ◽  
Albert Adhya ◽  
Shiying Zhang ◽  
Chi In Vong ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Function ◽  
Pulmonary Disease ◽  
Pulmonary Function Tests ◽  
Periodic Acid ◽  
Metabolic Reprogramming ◽  
Chronic Obstructive ◽  
Collagen Deposition ◽  
Obstructive Pulmonary Disease

Abstract Objectives Chronic obstructive pulmonary disease (COPD) remains a leading cause of death and treatment options for this condition remain scant. This study aims to examine the ability of γ-tocotrienol to mitigate disease progression in an animal model of COPD induced by e-cigarettes. We hypothesize that γ-tocotrienol will attenuate inflammation and subsequently slow the progression of e-cigarette induced COPD. Methods Scnn1b-Tg + mice (n = 10/group), were exposed to e-cigarette vapor twice daily for 10 days in an acute model and daily for eight weeks in a chronic model with or without γ-tocotrienol at a dose of 100 mg/kg/day. Following the treatment, animals underwent pulmonary function testing. Upon sacrifice, bronchoalveolar lavage (BAL) fluid and serum were collected for analysis of cytokine expression through cytokine array. Markers of oxidative stress, inflammation, and fibrosis in the lung were assessed via western blot. Mucus accumulation and structural changes (i.e., emphysema) were measured through Periodic Acid-Schiff and Hematoxylin and Eosin staining, respectively. Collagen deposition were evaluated by Sirius Red staining and Sircol Collagen assay. Cell morphology in BAL fluid was analyzed by Diff staining. Results In the acute model, γ-tocotrienol was evidenced to decrease collagen deposition and mucus accumulation in the bronchioles. Additionally, γ-tocotrienol reduced expression of cytokines C-X3-C motif chemokine ligand (CX3CL) 1 (P = 0.017), interleukin (IL) 4 (P = 0.0038) and T-cell immunoglobulin and mucin domain (TIM) 1 (P = 0.0215). Evidenced by large effect size, pulmonary function tests evidenced the ability of γ-tocotrienol to preserve lung function following 8 weeks of e-cigarette exposure. In addition, macrophage presence in BAL fluid was decreased following in mice supplemented with γ-tocotrienol following e-cigarette exposure. Conclusions Our results show the ability of γ-tocotrienol to attenuate the inflammatory response, and preserve lung function in models of e-cigarette induced COPD. These results indicate potential beneficial effects of γ-tocotrienol as an ancillary treatment in COPD. Funding Sources This work was supported by FAMRI foundation “METABOLIC REPROGRAMMING IN PATIENTS WITH COPD”, YCSA 2015.

Electroacupuncture inhibits IL-17/IL-17R and post-receptor MAPK signaling pathways in a rat model of chronic obstructive pulmonary disease

2021 ◽  
pp. 096452842199672
Author(s):  
Xin-Fang Zhang ◽  
Shui-Ying Xiang ◽  
Jing Lu ◽  
Yin Li ◽  
Shu-Jun Zhao ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Rat Model ◽  
Mapk Signaling ◽  
Chronic Obstructive ◽  
Inflammatory Infiltration ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α ◽  
Mapk Signaling Pathways

Objective: Interleukin (IL)-17, as a T-helper 17 cell (Th17) cytokine, plays a key role in chronic obstructive pulmonary disease (COPD) pathophysiology including chronic inflammation and airway obstruction, which lead to decreased pulmonary function. The aim of this study was to investigate the effect of acupuncture on IL-17, its receptor (IL-17R) and the mitogen-activated protein kinase (MAPK) signaling pathway, in a rat model of COPD. Methods: The COPD model was induced in Sprague Dawley rats by exposure to cigarette smoke for 12 weeks. The model rats were treated with electroacupuncture (EA) at BL13 and ST36. The lung function and histology of the rats were observed. IL-17, tumor necrosis factor (TNF)-α, and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA) in bronchoalveolar lavage fluid (BALF) and in plasma. The leukocytes and macrophages in the BALF were counted. The expression levels of IL-17R were assayed in lung tissue by real-time polymerase chain reaction (PCR), western blotting, and immunohistochemistry. MAPK signaling pathway molecules including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK)1/2 and p38, and their phosphorylated forms, were observed in the lung by western blotting. Results: Compared with the control group rats, lung function decreased and there was a severe inflammatory infiltration of the pulmonary parenchyma in the COPD rats. EA effectively improved lung function and alleviated the inflammatory infiltration in the lungs of COPD rats. EA also reversed the elevated total leukocyte and macrophage counts, the high levels of IL-17 and TNF-α, and the low IL-10 content in COPD rats. Meanwhile, EA downregulated the increased mRNA and protein expression of IL-17R, and significantly inhibited the elevated levels of phosphorylated JNK, ERK1/2, and p38 in the lungs of COPD rats. Conclusion: Our results suggest that the protective effects of acupuncture therapy on the lungs of COPD rats are likely related to inhibition of IL-17/IL-17R and the post-receptor MAPK signaling pathways.

scholarly journals Molecular Diagnosis of Intermediate and Severe α1-Antitrypsin Deficiency: MZ Individuals with Chronic Obstructive Pulmonary Disease May Have Lower Lung Function Than MM Individuals

2001 ◽  
Vol 47 (1) ◽  
pp. 56-62 ◽  
Author(s):  
Morten Dahl ◽  
Børge G Nordestgaard ◽  
Peter Lange ◽  
Jørgen Vestbo ◽  
Anne Tybjærg-Hansen
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Function ◽  
Pulmonary Disease ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Antitrypsin Deficiency ◽  
Lower Lung ◽  
Compound Heterozygotes

Abstract Background: We tested whether intermediate (MZ, SZ) and severe (ZZ) α1-antitrypsin deficiency affects lung function in the population at large. Methods: We performed spirometry [forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC)] and genotyping of 9187 individuals from the adult general population of Copenhagen, Denmark. Results: As expected, the frequencies of individuals with MM, MS, SS, MZ, SZ, and ZZ genotypes were 0.891, 0.054, 0.001, 0.052, 0.001, and 0.001, respectively. Genotype interacted with clinically established chronic obstructive pulmonary disease (COPD) on the percentage of the predicted FEV1 (P = 0.004): the percentage of the predicted FEV1 was reduced in MZ compared with MM individuals among those with clinically established COPD, but not among those without COPD. Furthermore, SZ compound heterozygotes had lower FEV1/FVC ratios than MM individuals (P &lt;0.05), and ZZ homozygotes had lower percentages of the predicted FEV1 and FEV1/FVC ratios than MM, MS, SS, and MZ individuals (all Ps &lt;0.01). Reduced lung function in SZ and ZZ vs MM individuals could be demonstrated in current and ex-smokers, but not in nonsmokers. Compared with MM individuals in the same groups, FEV1 was reduced 655 mL in MZ individuals with clinically established COPD, 364 mL in SZ current smokers, and 791 mL in ZZ current smokers. Conclusions: In the population at large, MZ was associated with reduced pulmonary function in individuals with clinically established COPD, whereas SZ and ZZ were associated with reduced pulmonary function in smokers. The presence of the α1-antitrypsin MZ genotype may in certain circumstances produce marked aggravation of airway obstruction in individuals prone to develop COPD.

scholarly journals Long-Term Effects of Acupuncture Treatment on Airway Smooth Muscle in a Rat Model of Smoke-Induced Chronic Obstructive Pulmonary Disease

2016 ◽  
Vol 34 (2) ◽  
pp. 107-113 ◽  
Author(s):  
Jia Li ◽  
Song Wu ◽  
Hongtu Tang ◽  
Wei Huang ◽  
Lushan Wang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Function ◽  
Pulmonary Disease ◽  
Rat Model ◽  
Acupuncture Treatment ◽  
Chronic Obstructive ◽  
Long Term Effects ◽  
Obstructive Pulmonary Disease ◽  
Histone Deacetylase 2 ◽  
Tnf Α

Background Chronic obstructive pulmonary disease (COPD) is one of the most common lung diseases. It is a chronic inflammatory process characterised by airway obstruction and progressive lung inflammation, associated with difficulty breathing and insensitivity to corticosteroid therapy. Although there is some preliminary evidence to suggest a beneficial effect of acupuncture on COPD, its mechanism of action has not been investigated. Our aim was to examine the anti-inflammatory effects of acupuncture in a rat model of COPD induced by exposure to cigarette smoke (CS). Methods Sixty Sprague–Dawley rats were exposed to the smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months to induce COPD and treated with acupuncture at BL13 ( Feishu), BL23 ( Shenshu) and Dingchuan (COPD+Acupuncture, n=15), sham acupuncture (COPD+Sham, n=15) or left untreated (n=15). Exposed rats were compared with controls not exposed to CS (control, n=15). Pulmonary function was measured, and tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8) levels were determined in bronchoalveolar lavage fluid by ELISA. Histone deacetylase 2 (HDAC2) protein and mRNA expression were examined in lung tissue and in bronchus. Results Acupuncture treatment appeared to protect pulmonary function and reduce the COPD-induced inflammatory response by decreasing cell inflammation and the production of TNF-α and IL-8. Acupuncture also enhanced HDAC2 mRNA and protein expression, suggesting a possible direct effect on protein structure through post-translational modifications. Conclusions Our results suggest that acupuncture regulates inflammatory cytokines and contributes to lung protection in a rat model of smoke-induced COPD by modulating HDAC2.

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