Regulatory Effects of Andrographolide on Lung Tissue Inflammation and Th17/Treg in Rats with Chronic Obstructive Pulmonary Disease Induced by Smoking and Lipopolysaccharide

The pathogenesis of Chronic obstructive pulmonary disease (COPD) is complex, and lung tissue inflammation and Th17/Treg imbalance are the key factors causing lung dysfunction. We constructed a rat COPD model induced by smoking and lipopolysaccharide to explore andrographolide’s regulation on lung inflammation and Th17/Treg in COPD rats. By contrast, the study found that normal rats, COPD rats forced expiratory volume of 0.3 seconds (FEV 0 . 3 ), FEV 0.3 /forced vital capacity (FVC), and peak expiratory flow (PEF) levels decreased. In addition, the levels of IL-8, TNF-α, IL-17, and IL-6 in alveolar lavage fluid increased, and the level of IL-10 decreased. Concurrently, the total number of white blood cells, monocytes and macrophages, neutrophils, and lymphocytes increased. Meanwhile, the contents of CD25, CD4, and Foxp3 in lung tissue all increased, and the protein levels of HMGB1, TLR4, and p65 increased. After treatment with andrographolide, the levels of FEV 0.3 , FEV 0.3 /FVC, and PEF increased, proving the increase was positively correlated with the concentration of andrographolide. The levels of IL-8, TNF-α, IL-17, and IL-6 in rat alveolar lavage fluid decreased, and the level of IL-10 sequentially. The total number of white blood cells, the number of monocytes and macrophages, the number of lymphocytes, and the neutral Granulocytes decreased significantly. And the contents of CD25, CD4, and Foxp3 in lung tissue significantly decreased, and the protein levels of HMGB1, TLR4, and p65 significantly decreased. The above results indicate that andrographolide might be a potential COPD treatment approach. Andrographolide improves the lung function of rats with COPD, reduces lung inflammation, regulates Th17/Treg balance, and its mechanism may be related to HMGB1/TLR4/NF-кB signaling.