河北医学2025，Vol.31Issue(12)：1937-1943,7.DOI:10.3969/j.issn.1006-6233.2025.12.01
miR-98-5p调控STAT3对过敏性鼻炎小鼠炎症反应的影响
Effect of miR-98-5p on Inflammatory Response of Allergic Rhinitis Mice by Regulating STAT3
摘要
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 na-sal 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.West-ern 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 struc-ture.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 visi-ble.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,apopto-sis 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 mR-NA 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,eosin-ophils,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.关键词
过敏性鼻炎/微小RNA-98-5p/信号转导和转录激活因子3/炎症反应Key words
Allergic rhinitis/MicroRNA-98-5p/Signal transducer and activator of transcription 3/Inflammatory response引用本文复制引用
吴雄英,胡婷,李鹏程..miR-98-5p调控STAT3对过敏性鼻炎小鼠炎症反应的影响[J].河北医学,2025,31(12):1937-1943,7.基金项目
湖北省自然科学基金,(编号:2020HBA216) （编号:2020HBA216）
