The present in vitro analysis confirmed that PW root extract (PWRE) exerts anti‑inflammatory effects in phorbol myristate acetate‑ or tumor necrosis factor α (TNF‑α)‑stimulated human lung epithelial NCI‑H292 cells by attenuating the expression of interleukin (IL)‑8, IL‑6 and Mucin A5 (MUC5AC), which are closely associated with the pulmonary inflammatory response in the pathogenesis of COPD.
Compared with the expression levels in the non-smokers and smokers without COPD, CD147 and MUC5AC expression levels were higher in the smokers with COPD.
Airway mucus hypersecretion is one of the most serious pathophysiological symptoms of chronic airway inflammatory diseases, and the human mucin 5AC (MUC5AC) gene has been reported to be a major component of respiratory secretions related to asthma and chronic obstructive pulmonary disease.
In addition, we preliminarily confirmed TAS-203 prevents airway MUC5AC production in BAL fluid, and shows lower specific airway resistance (sRaw) in a cigarette smoke-induced COPD-like model.
MicroRNA-218 acts by repressing TNFR1-mediated activation of NF-κB, which is involved in MUC5AC hyper-production and inflammation in smoking-induced bronchiolitis of COPD.
The absolute concentrations of MUC5B and MUC5AC in current or former smokers with severe COPD were approximately 3 times as high and 10 times as high, respectively, as in controls who had never smoked.
The manifest and important feature in respiratory diseases, including asthma and COPD (chronic obstructive pulmonary disease), is the increased numbers and hypersecretion of goblet cells and overexpression of mucins, especially Muc5ac.
These data taken together demonstrate that Egr-1 is essential for CSE-induced MUC5AC production in HBE cells likely through interaction with and modulation of AP-1, and re-emphasize targeting Egr-1 as a novel therapeutic strategy for COPD.
The lungs from CS rats were pathologically similar to those of COPD patients with the characteristics of goblet cell metaplasia and MUC5AC hypersecretion.
Smoking attenuated the expressions of AQP5 and increased the staining of MUC5AC and mucus in submucosal glands in the COPD groups (P<0.01), while there were no significant differences observed in the control group (P>0.05).
Samples from COPD showed a stronger staining for MUC5AC than those in control subjects (P < 0.01) and AB-PAS staining revealed more mucins in COPD patients' submucosal gland comparing with that in control subjects (P < 0.01).