Asthma is a chronic inflammatory disorder of the airways. Schisandrin B (SB) is the main effective component. This study investigated the effects of SB on airway inflammation and airway remodeling in asthma. The rat model of asthma was established. The rats were treated with SB to evaluate the effects of SB on airway inflammation, airway remodeling, NLRP3 inflammasome activation, and pyroptosis. Alveolar macrophages of rats were isolated, and the macrophage inflammatory model was established by lipopolysaccharide (LPS) induction. The LPS-induced macrophages were treated with SB. The binding relationship between miR-135a-5p and TPRC1 was analyzed. LPS + SB-treated macrophages were transfected with miR-135a-5p inhibitor. The expressions of key factors of the STAT3/NF-κB pathway were detected. SB reduced airway inflammation and airway remodeling in asthmatic rats. SB inhibited NLRP3 inflammasome activation and reduced pyroptosis in asthmatic rats and LPS-induced macrophages. SB reversely regulated the miR-135a-5p/TRPC1 axis. Downregulation of miR-135a-5p attenuated the inhibitory effect of SB on NLRP3 inflammasome activation. SB inhibited the STAT3/NF-κB pathway via the miR-135a-5p/TRPC1 axis. In conclusion, SB inhibited NLRP3 inflammasome activation and reduced pyroptosis via the miR-135a-5p/TRPC1/STAT3/NF-κB axis, thus alleviating airway inflammation and airway remodeling in asthma. This study may confer novel insights for the management of asthma.

哮喘是一种慢性气道炎症性疾病。五味子乙素（SB）是主要有效成分。本研究调查了 SB 对哮喘气道炎症和气道重塑的影响。建立大鼠哮喘模型。用SB治疗大鼠以评估SB对气道炎症、气道重塑、NLRP3炎性体激活和细胞焦亡的影响。分离大鼠肺泡巨噬细胞，通过脂多糖（LPS）诱导建立巨噬细胞炎症模型。 LPS诱导的巨噬细胞用SB处理。分析miR-135a-5p与TPRC1之间的结合关系。 LPS + SB 处理的巨噬细胞用 miR-135a-5p 抑制剂转染。检测STAT3/NF-κB通路关键因子的表达。 SB 可减少哮喘大鼠的气道炎症和气道重塑。 SB 抑制 NLRP3 炎性体激活并减少哮喘大鼠和 LPS 诱导的巨噬细胞的细胞焦亡。 SB 反向调节 miR-135a-5p/TRPC1 轴。 miR-135a-5p 的下调减弱了 SB 对 NLRP3 炎性体激活的抑制作用。 SB 通过 miR-135a-5p/TRPC1 轴抑制 STAT3/NF-κB 通路。总之，SB 通过 miR-135a-5p/TRPC1/STAT3/NF-κB 轴抑制 NLRP3 炎症小体激活并减少细胞焦亡，从而减轻哮喘气道炎症和气道重塑。这项研究可能为哮喘的治疗提供新的见解。