首页|基于TLR4/MyD88/NF-κB通路探讨加味过敏煎对抗生素加重过敏性哮喘小鼠的抗炎机制

基于TLR4/MyD88/NF-κB通路探讨加味过敏煎对抗生素加重过敏性哮喘小鼠的抗炎机制

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目的:探讨加味过敏煎对抗生素加重过敏性哮喘小鼠的干预作用及潜在作用机制.方法:将40只雄性BALB/c小鼠随机分为空白组、模型组(抗生素加重过敏性哮喘组)、中药组(加味过敏煎组,6.3 g·kg-1)、西药组(匹多莫德联合氨茶碱组,给予匹多莫德0.0378 g·kg-1+氨茶碱0.2 g·kg-1),每组10只.采用卵清蛋白(OVA)和氢氧化铝凝胶佐剂结合OVA雾化激发的方法建立过敏性哮喘小鼠模型,头孢哌酮舒巴坦钠滴鼻建立抗生素加重过敏性哮喘小鼠模型.雾化激发前30 min灌胃给药,连续给药7 d后检测小鼠肺组织病理变化;ELISA法检测小鼠血清中IgE、IL-4、IL-5、IL-13表达水平;Western blot法检测小鼠肺组织中TLR4、MyD88、p-NF-κB p65蛋白表达水平.结果:与空白组相比,抗生素加重过敏性哮喘组支气管结构重度异常,部分支气管上皮细胞脱落,其中还有大量蛋白黏液渗出,支气管周围见大量炎性细胞浸润,肺泡壁明显增厚,肺泡萎缩;血清中IgE、IL-4、IL-5、IL-13水平升高(P<0.01);TLR4、MyD88、p-NF-κB p65蛋白表达升高(P<0.01);与抗生素加重过敏性哮喘组相比,加味过敏煎组小鼠支气管结构正常,肺泡壁增厚情况显著改善,炎性细胞浸润减轻;血清中IgE、IL-4、IL-5、IL-13 水平显著下降(P<0.01);TLR4、MyD88、p-NF-κB p65 蛋白表达明显降低(P<0.01).结论:加味过敏煎可改善抗生素加重过敏性哮喘气道炎症情况,其作用机制可能与调控TLR4/MyD88/NF-κB通路有关.
Exploration of the Anti-Inflammatory Mechanism of Jiawei Guomin Decoction on Antibiotic-Exacerbated Allergic Asthma in Mice Based on the TLR4/MyD88/NF-κB Pathway
Objective:To investigate the intervention effect and potential mechanism of Jiawei Guomin Decoction on antibiotic-exacerbated allergic asthma in mice.Methods:Forty male BALB/c mice were randomly divided into four groups:a blank group,a model group(antibiotic-exacerbated allergic asthma group),a traditional Chinese medicine group(Jiawei Guomin Decoction group,6.3 g·kg-1),and a Western medicine group(Pidotimod 0.0378 g·kg-1+theophylline 0.2 g·kg-1),with 10 mice per group.Allergic asthma mouse model was established using ovalbumin(OVA)and aluminum hydroxide gel adjuvant combined with OVA nebulization,and antibiotic-exacerbated allergic asthma model was established by nasal instillation of cefoperazone and sulbactam sodium.Drugs were administered by gavage 30 minutes before nebulization for 7 days,and the mice were then assessed for lung tissue pathology.ELISA was used to measure serum levels of IgE,IL-4,IL-5,and IL-13;Western blot was used to detect protein expression levels of TLR4,MyD88,and p-NF-κBp65 in lung tissue.Results:Compared to the normal group,the antibiotic-exacerbated allergic asthma group exhibited severe abnormalities in bronchial structure,shedding of some bronchial epithelial cells,significant protein mucus exudation,extensive inflammatory cell infiltration around the bronchi,thickened alveolar walls,and alveolar atrophy.Serum levels of IgE,IL-4,IL-5,and IL-13 were elevated(P<0.01);TLR4,MyD88,and p-NF-κBp65 protein expressions were increased(P<0.01).Compared to the antibiotic-exacerbated allergic asthma group,the Jiawei Guomin Decoction group showed normal bronchial structure,significantly improved alveolar wall thickening,and reduced inflammatory cell infiltration.Serum levels of IgE,IL-4,IL-5,and IL-13 were significantly decreased(P<0.01);TLR4,MyD88,and p-NF-κBp65 protein expressions were markedly reduced(P<0.01).Conclusion:Jiawei Guomin Decoction can improve airway inflammation in antibiotic-exacerbated allergic asthma,and its mechanism may be related to the regulation of the TLR4/MyD88/NF-κB signaling pathway.

Antibiotic-exacerbated allergic asthmaTLR4/MyD88/NF-κB pathwayAirway inflammationJiawei Guomin Decoction

杨爽、王亚楠、黄燕

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内蒙古自治区中医医院,内蒙古呼和浩特 010050

鄂伦春自治旗宜里镇中心卫生院,内蒙古呼伦贝尔 165474

抗生素加重过敏性哮喘 TLR4/MyD88/NF-κB通路 气道炎症 加味过敏煎

2025

中医药学报
中华中医药学会,黑龙江中医药大学

中医药学报

影响因子:1.169
ISSN:1002-2392
年,卷(期):2025.53(1)