A total of 48 C57BL/6 mice were divided into control group，SB group， COPD group， and COPD+SB group， and there were 12 mice in each group. The mice in COPD group and COPD+SB group were given cigarette smoke and lipopolysaccharide （LPS） to establish the COPD models. The airway resistance after inhalation of methacholine （Mch） was observed to evaluate the lung function of the mice in various groups， and the pathomophology of lung tissue of the mice in various groups was observed by HE staining. The total number of white blood cells， neutrophils， macrophages and lymphocytes， the levels of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and interleukin-18 （IL-18） in pulmonary alveolar lavage fluid （BALF） of the mice in various groups were detected by cell counting and ELISA method.The mouse macrophage RAW264.7 cells were stimulated by cigaritte smoke extract （CSE） in vitro， and the cells were divided into control group， SB group， CSE group and SB+CSE group. Cell immunofluorescence staining was used to observe the expressions of NOD-like receptor protein 3（NLRP3） and cleaved caspase-3 in the macrophages in various groups， and flow cytometry was used to detect the pyroptotic rates and early apoptotic rates of the cells in various groups，and Western blotting method was used to detect the expression levels of phosphorylated p-38（p-p-38），pyroptosis-related and nuclear factor κB（NF-κB） signaling pathway related poteins in the macrophages in various groups.

The COPD mouse models were successfully established.Compared with control group， the airway resistance of the mice in COPD group and COPD+SB group， the total number of white blood cells， neutrophils， macrophages and lymphocytes in BALF， the levels of TNF-α， IL-6， IL-1β ，IL-18 in BALF， and the expression levels of p-p-38， NLRP3，cysteine protease 1（caspase-1），apoptosis-associated spotted protein（ASC），NF-κB p65，and Toll-like receptor 4 （TLR4） proteins in lung tissue of the mice were increased （P<0.05 or P<0.01）；the lung tissue was obviously damaged， the airway epithelial cells were exfoliated， and some adjacent alveoli fused to bullae.Compared with control group， the airway resistance of the mice in SB group， the total number of white blood cells， neutrophils， macrophages and lymphocytes in BALF， the levels of TNF-α， IL-6， IL-1β ，and IL-18 in BALF， and the expression levels of NLRP3， caspase-1， ASC， NF-κB p65， and TLR4 proteins in lung tissue had no significant differences（P>0.05）； the lung tissue was normal， but the expression level of p-p-38 in lung tissue was significantly decreased （P<0.05）. Compared with COPD group， the airway resistance of the mice in COPD+SB group， the total number of white blood cells， neutrophils， macrophages and lymphocytes in BALF， the levels of TNF-α， IL-6， IL-1β， and IL-18 in BALF， and the expression levels of NLRP3， caspase-1， ASC， NF-κB p65，and TLR4 proteins were decreased（P<0.05）；the pathological injury of lung tissue of the mice in COPD+SB group was alleviated（P<0.05）. In vitro experiments， compared with control group， the expression amounts of NLRP3 and cleaved caspase-3， pyroptotic rates and early apoptotic rates of the cells， the expression levels of p-p-38， ASC， NF-κB p65， TLR4， and cleaved caspas-3 proteins in the macrophages in CSE group and CSE+SB group were increased （P<0.05 or P<0.01）；the pyroptotic rate and early apoptotic rate of the cells， and expression levels of NLRP3， cleaved caspase-3， ASC， NF-κB p65， TLR4， and cleaved caspase-3 proteins in the macrophages in SB group had no significant differences（P>0.05）， and the expression level of p-p-38 in SB group was decreased （P<0.05）. Compared with CSE group， the early apoptotic rate of the macrophages and the expression level of cleaved caspase-3 in the cells in CSE+SB group were increased （P<0.05），and the pyroptotic rate， the expression levels of p-p-38， NLRP3， ASC， NF-κB p65，TLR4， and cleaved caspase-3 proteins were decreased （P<0.05）.

SB may improve the lung injury and inflammatory response of COPD by inhibiting the pyroptosis of macrophages mediated by the NLRP3 pathway.