To explore the omalizumab via microRNA (miR)-26a-5p reduced the inflammasome, or the NOD-like receptor themal domain associated protein 3 (NLRP3) mediated pyroptosis on airway remodeling in asthmatic rats, based on the inhibition of the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response protein 88 (MyD88)/nuclear factor kappa-B (NF-κB) signaling pathway.

Fifty SD rats were divided into control group, model group, omalizumab group, omalizumab+agomir NC group and omalizumab+miR-26a-5p agomir group, with 10 rats in each group. The control group was intraperitoneally injected with 0.9% NaCl; the model group established the asthma model; the omalizumab group was intraperitoneally injected with 100 mg·kg^-1·d^-1 omalizumab daily on the basis of model group; the omalizumab + agomir NC group received tail vein injection of agomir NC on the basis of the omalizumab group; the omalizumab+ miR-26a-5p agomir group received tail vein injection of miR-26a-5p agomir on the basis of omalizumab group. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissue; enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of inflammatory factors; real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) and fluorescence in situ hybridization (FISH) were used to detect the expression of miR-26a-5p; Western blotting (WB) was used to detect the pyroptosis and TLR4/MyD88/NF -κB pathway-related proteins expression levels.

The tube wall thickness in control group, model group and omalizumab group were (35.16±2.95), (52.94±4.63) and (44.07±3.78) μm; interleukin-13 (IL-13) levels were (18.23±3.94), (61.84±10.94) and (34.23±6.11) pg·mL^-1; interferon gamma (IFN-γ) levels were (68.43±11.59), (22.94±4.70) and (43.10±8.04) pg·mL^-1; miR-26a-5p mRNA were 1.00±0.15, 2.26±0.31 and 1.37±0.19. The relative expression levels of NLRP3 in control group, the model group, the omalizumab group, the omalizumab +agomir NC group and omalizumab+miR-26a-5p agomir group were 1.00±0.11, 3.21±0.47, 1.77±0.24, 1.69±0.27 and 2.53±0.38; the relative expression levels of TLR4 were 1.00±0.13, 2.54±0.39, 1.86±0.39, 1.90±0.30 and 2.24±0.34; the relative expression levels of MyD88 were 1.00±0.15, 1.97±0.26, 1.44±0.21, 1.41±0.18 and 1.69±0.23; the relative expression levels of NF-κB were 1.00±0.12, 2.88± 0.37, 1.83±0.29, 1.77±0.25 and 2.54±0.41, respectively. The differences of the above indexes were statistically significant when compared the model group with the control group, the omalizumab group with the model group, and the omalizumab+miR-26a-5p agomir group with the omalizumab+agomir NC group (P<0.05, P<0.01).

Omalizumab may reduce NLRP3 inflammasome-mediated pyroptosis by inhibiting the activation of TLR4/MyD88/NF-κB pathway, thus achieving omalizumab inhibited airway remodeling and improved lung function in bronchial asthmatic rats.