scholarly journals Buyuan decoction inhibits autophagy in a rat model of chronic obstructive pulmonary disease

2021 ◽  
pp. 47-47
Author(s):  
Chunyan Huang ◽  
Shaofeng Li ◽  
Chao Xu ◽  
Wenlong Song ◽  
Lei Xu ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Experimental Model ◽  
Lung Tissue ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
High Dose ◽  
Sprague Dawley ◽  
Obstructive Pulmonary Disease ◽  
Transmission Electron

Efforts have been made to find a better therapeutic approach with fewer side effects in treating chronic obstructive pulmonary disease (COPD). This study investigated the effect of Buyuan decoction (BYD) on autophagy in COPD rats. An experimental model with Sprague-Dawley rats was established by lipopolysaccharide (LPS) injection and cigarette smoke exposure. Rats were randomly allocated into blank control (normal control), experimental model, low-dose BYD (8.0 g/kg/day), medium-dose BYD (16.0 g/kg/day), high-dose BYD (32.0 g/kg/day) and 3-MA (methyladenine) groups (6 rats/group). Cell and tissue morphology were observed using hematoxylin and eosin staining. Autophagic vesicles were examined with a transmission electron microscope. Protein expression of LC3-II/I, BNIP-1, ATG7, p62, PI3K and p-PI3K in lung tissue was detected by Western blotting. Compared with the experimental model group, the inflammatory infiltrate in lung tissue was reduced, the nuclei of the pulmonary epithelial cells were restored to normal, and the expression of LC3, BNIP1, ATG7 and p-PI3K was significantly downregulated, while p62 expression was significantly upregulated after treatment with the BYD. The effect was most significant in the lowdose BYD group (P<0.05, all groups). These findings suggest that the BYD inhibits the occurrence of autophagy in the pathogenesis of COPD and that it can be a potential treatment.

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 Low-Level Laser Therapy Reduces Lung Inflammation in an Experimental Model of Chronic Obstructive Pulmonary Disease Involving P2X7 Receptor

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Gabriel da Cunha Moraes ◽  
Luana Beatriz Vitoretti ◽  
Auriléia Aparecida de Brito ◽  
Cintia Estefano Alves ◽  
Nicole Cristine Rigonato de Oliveira ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Laser Therapy ◽  
Experimental Model ◽  
P2x7 Receptor ◽  
Low Level Laser Therapy ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Low Level Laser ◽  
Level Laser

Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by irreversible airflow limitation, airway inflammation and remodeling, and enlargement of alveolar spaces. COPD is in the top five leading causes of deaths worldwide and presents a high economic cost. However, there are some preventive measures to lower the risk of developing COPD. Low-level laser therapy (LLLT) is a new effective therapy, with very low cost and no side effects. So, our objective was to investigate if LLLT reduces pulmonary alterations in an experimental model of COPD. C57BL/6 mice were submitted to cigarette smoke for 75 days (2x/day). After 60 days to smoke exposure, the treated group was submitted to LLLT (diode laser, 660 nm, 30 mW, and 3 J/cm2) for 15 days and euthanized for morphologic and functional analysis of the lungs. Our results showed that LLLT significantly reduced the number of inflammatory cells and the proinflammatory cytokine secretion such as IL-1β, IL-6, and TNF-α in bronchoalveolar lavage fluid (BALF). We also observed that LLLT decreased collagen deposition as well as the expression of purinergic P2X7 receptor. On the other hand, LLLT increased the IL-10 release. Thus, LLLT can be pointed as a promising therapeutic approach for lung inflammatory diseases as COPD.

scholarly journals Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 184 (8) ◽  
pp. 4460-4469 ◽  
Author(s):  
Gregory T. Motz ◽  
Bryan L. Eppert ◽  
Brian W. Wortham ◽  
Robyn M. Amos-Kroohs ◽  
Jennifer L. Flury ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mouse Model ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Cell Activation ◽  
Nk Cell ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease
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