Abstract：Objective: To explore the effect of microRNA-98-5p (miR-98-5p) on the inflammatory response of allergic rhinitis (AR) mice by regulating the signal transducer and activator of transcription 3 (STAT3). Methods: The dual luciferase reporter gene assay was used to determine the targeting relationship between miR-98-5p and STAT3. An AR mouse model induced by ovalbumin (OVA) was constructed, and successfully modeled mice were randomly assigned into AR group, NC agomir group (tail vein injection of NC agomir), miR-98-5p agomir group (tail vein injection of miR-98-5p agomir), and Garcinone D (tail vein injection of miR-98-5p agomir+1mg/kg STAT3 activator Garcinone D), each consisting of 10mice. Another 10mice were included as the control group, and equal amounts of physiological saline were injected into the control group and AR group, respectively. The mice in each group were evaluated for AR symptoms. ELISA was used to measure IgE and inflammatory cytokines in mouse serum. The number of inflammatory cells in nasal lavage fluid (NALF) was detected. The qRT-PCR method was performed to detect miR-98-5p and STAT3 mRNA in the nasal mucosal tissue of AR mice. HE staining was performed to measure the pathology of nasal mucosal tissue. TUNEL staining was performed to measure apoptosis of nasal mucosal tissue cells. Western blot was used to detect STAT3 and Cleaved Caspase-3 proteins in nasal mucosal tissue. Results: MiR-98-5p could target negative regulation of STAT3. The control group had intact nasal mucosal epithelial structure. The nasal mucosal epithelial tissue of the AR group and NC agomir group showed obvious defects, with enlarged intercellular spaces and abundant infiltration of inflammatory cells. The miR-98-5p agomir group showed obvious improvement in nasal mucosal injury, with a small amount of inflammatory cell infiltration visible. Garcinone D group further aggravated nasal mucosal damage and increased inflammatory cell infiltration. The AR group had higher AR symptom scores, lymphocytes, macrophages, eosinophils, neutrophils, apoptosis rate, IgE, IL-4, IL-5, IL-13, STAT3 mRNA and protein, Cleaved Caspase-3, and lower miR-98-5p and IFN-γ than the control group (P<0.05). The miR-98-5p agomir group had lower AR symptom scores, lymphocytes, macrophages, eosinophils, neutrophils, apoptosis rate, IgE, IL-4, IL-5, IL-13, STAT3 mRNA and protein, Cleaved Caspase-3, and higher miR-98-5p and IFN-γ than the AR group and NC agomir group (P<0.05). The Garcinone D group had higher AR symptom scores, lymphocytes, macrophages, eosinophils, neutrophils, apoptosis rate, IgE, IL-4, IL-5, IL-13, STAT3 mRNA and protein, Cleaved Caspase-3, and lower IFN-γ than the miR-98-5p agomir group (P<0.05). Conclusion: MiR-98-5p may inhibit the inflammatory response in AR mice by regulating STAT3.
2025, Vol. 31 
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