Objective To explore the effect of lncRNA TUG1 on airway smooth muscle cell apoptosis and inflammatory factors in children with asthma and its molecular mechanism. Methods The airway smooth muscle tissues of children with bronchial asthma and non-asthma patients who were admitted to our hospital from January 2017 to June 2020 were collected; airway smooth muscle cells (ASMCs) were isolated and cultured; and divided into si-NC group, si-TUG1 group, miR-mimics-NC group, miR-326mimics group, si=NC+miR-inhibitor-NC group, si-TUG1+miR-inhibitorNC group, s-TUG1+miR-326 inhibitor group. Real-time fluorescence quantitative PCR (RT-qPCR) to detect the expression levels of TUG1 and miR-326; flow cytometry to detect cell apoptosis. Western blot to detect protein expression. The enzymelinked immunosorbent assay (ELISA) to detect IL-4, IL-5, IL-13 levels. The dual luciferase report experiments verify the targeting relationship between TUG1 and miR-326. Results The expression of TUG1 in airway smooth muscle tissue of asthmatic patients was increased, and the expression of miR-326 was decreased (P＜0.05). After silencing lncRNA TUG1 or overexpressing miR-326, the apoptosis rate in ASMCs was increased, the expressionof Bcl-2 was decreased, the expression of Bax was increased, and the levels of IL-4, IL-5 and IL-13 were decreased(P＜0.05). TUG1 targets and negatively regulates miR-326; interference with miR-326 can reverse the effect of silencing TUG1 on airway smooth muscle cell apoptosis and inflammatory factors. Conclusion Silencing lncRNA TUG1 can promote the apoptosis of airway smooth muscle cells in children with asthma and inhibit the release of inflammatory factors by targeted regulation of miR-326.