Protective effect of exogenous hydrogen sulfide on pulmonary artery endothelial cells by suppressing endoplasmic reticulum stress in a rat model of chronic obstructive pulmonary disease

2018 ◽  
Vol 105 ◽  
pp. 734-741 ◽  
Author(s):  
Hai-Bo Ding ◽  
Kai-Xiong Liu ◽  
Jie-Feng Huang ◽  
Da-Wen Wu ◽  
Jun-Ying Chen ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Hydrogen Sulfide ◽  
Endoplasmic Reticulum Stress ◽  
Pulmonary Artery ◽  
Protective Effect ◽  
Rat Model ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

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 Function of monocytes and monocyte-derived macrophages in α1-antitrypsin deficiency

2014 ◽  
Vol 45 (2) ◽  
pp. 365-376 ◽  
Author(s):  
Emily F.A. van’t Wout ◽  
Annemarie van Schadewijk ◽  
David A. Lomas ◽  
Jan Stolk ◽  
Stefan J. Marciniak ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Endoplasmic Reticulum Stress ◽  
Genetic Disorder ◽  
Nuclear Factor Κb ◽  
Endoplasmic Reticulum Stress Response ◽  
Local Source ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Antitrypsin Deficiency

α1-antitrypsin deficiency is the most widely recognised genetic disorder causing chronic obstructive pulmonary disease (COPD). Mutant Z α1-antitrypsin expression has previously been linked to intracellular accumulation and polymerisation of this proteinase inhibitor. Subsequently, this has been described to underlie an exaggerated endoplasmic reticulum stress response and enhanced nuclear factor-κB signalling. However, whether monocyte-derived macrophages display the same features remains unknown.Monocytes from homozygous PiZZ α1-antitrypsin deficiency patients and PiMM controls were cultured for 6 days in the presence of granulocyte-macrophage or macrophage colony-stimulating factor to obtain pro- and anti-inflammatory macrophages (mφ-1 and mφ-2, respectively).We first showed that, in contrast to monocytes, pre-stressed mφ-1 and mφ-2 from healthy blood donors display an enhanced endoplasmic reticulum stress response upon a lipopolysaccharide trigger (XBP1 splicing, CHOP, GADD34 and GRP78 mRNA). However, this endoplasmic reticulum stress response did not differ between monocyte-derived macrophages and monocytes from ZZ patients compared to MM controls. Furthermore, these ZZ cells do not secrete higher cytokine levels, and α1-antitrypsin polymers were not detectable by ELISA.These data suggest that monocyte-derived macrophages are not the local source of Z α1-antitrypsin polymers found in the lung and that endoplasmic reticulum stress and pro-inflammatory cytokine release is not altered.

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