OBJECTIVE To explore the improvement effects of Suting pingchuan decoction （STPC） on bronchial asthma in rats and its potential mechanism. METHODS Male SD rats were randomly divided into blank group， model group， STPC low-， medium- and high-dose groups （4.14， 8.28， and 16.56 g/kg， respectively， based on the crude drug dosage）， and dexamethasone group （positive control， 1 mg/kg）， with 8 rats in each group. Except for the blank group， the other groups were sensitized by intraperitoneal injection of ovalbumin and challenged by nebulized inhalation of ovalbumin to establish a bronchial asthma model. From the day of nebulization challenge， rats of each group were administered the corresponding drug solution or normal saline by gavage 1 hour before aerosolization， once a day， for 7 consecutive days. During the experiment， behavioral changes in rats of each group were observed. After the last administration， the levels of inflammatory factors （interleukin-1β， interleukin-18） in bronchoalveolar lavage fluid （BALF）， and oxidative stress indexes [malondialdehyde （MDA）， superoxide dismutase （SOD）] in lung tissue were determined； pathological changes in lung tissue were observed； cell apoptosis in lung tissue， and the mRNA expression of nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3） and the protein expressions of NLRP3， cleaved caspase-1， caspase-1， gasdermin D （GSDMD） and gasdermin D-N-terminal domain （GSDMD-N） in lung tissue were detected. RESULTS Compared with the blank group， rats in the model group showed symptoms such as scratching their ears and noses and frequent sneezing； the lung tissue structure was severely damaged， and there was obvious inflammatory cell infiltration. The levels of inflammatory factors in BALF， as well as the level of MDA， TUNEL-apoptotic cell rate， the mRNA expression of NLRP3， and the protein expressions of NLRP3， cleaved caspase-1， caspase-1， GSDMD-N and GSDMD in lung tissue were significantly increased or up-regulated， while the level of SOD in lung tissue was significantly decreased （ P ＜0.05 or P ＜0.01）. Compared with the model group， the above symptoms and pathological damages of lung tissue in each drug group were significantly improved， and all quantitative indicators （except for the protein expressions of GSDMD in the STPC groups， as well as the level of SOD， and the protein expressions of cleaved caspase-1， caspase-1 and GSDMD-N in the STPC low-dose group） were significantly reversed （ P ＜0.05 or P ＜0.01）. CONCLUSIONS STPC can improve airway inflammation and lung tissue damage in rats with bronchial asthma， reduce the level of oxidative stress， and decrease the release of inflammatory factors such as IL-1β and IL-18. Its mechanism of action may be related to the inhibition of pyroptosis activation mediated by the NLRP3/caspase-1/GSDMD signaling pathway.