摘要
目的:使用和厚朴酚(HNK)干预哮喘小鼠模型,分析HNK对气道炎症的影响,并探讨其机制。方法:选取20只6周龄健康雌性C57BL/6J小鼠,随机分为空白对照组(CTRL组)、哮喘模型组(OVA组)、地塞米松治疗组(DXM组)、和厚朴酚干预组(HNK组)。采用鸡卵清蛋白(OVA)+氢氧化铝[Al(OH)_(3)]构建经典哮喘模型,激发过程中DXM组小鼠腹腔内注射DXM溶液,HNK组小鼠腹腔内注射HNK溶液,CTRL组小鼠使用等量生理盐水。检测各组小鼠气道高反应性、肺组织炎症细胞浸润情况、细胞学分类计数、血清炎症因子表达水平及肺组织氧化应激因子水平。结果:HNK干预后,各组小鼠气道高反应性、血清炎症因子水平、肺组织氧化应激因子水平均降低,细胞学分类计数减少,差异均有统计学意义(P<0.05)。结论:在哮喘小鼠模型中,HNK可以通过抑制氧化应激反应,减轻气道炎症反应。
Objective:It investigated the protective actions of Honokiol on lung inflammation of asthma mice and analyzed its related mechanism.Methods:Twenty 6-week-old healthy female C57BL/6J mice were selected and randomly divided into control(CTRL)group,ovalbumin(OVA)group,dexamethasone(DXM)group,and magnolol(HNK)group.The classic asthma mice model was constructed with OVA+Al(OH)_(3).During stimulation process,mice of the DXM group were injected with dexamethasone solution intraperitoneally while mice of HNK group were injected with Honokiol solution intraperitoneally.Mice of CTRL group were given an equal amount of PBS.It detected airway hyperresponsiveness,inflammatory cell infiltration status,cytology classification of BALF,and the expression and oxidative stress level of serum inflammatory factors in different groups.Results:After the intervention,the airway inflammation,serum,inflammation factor level of mice,and the lung oxidative stress were decreased,the cytology classification was decreased,and the differences were statistically significant.Conclusion:Honokiol can release lung inflammation by inhibiting oxidative stress in asthma mice.
作者
唐大春
刘小高
戴曦
Tang Dachun;Liu Xiaogao;Dai Xi(Department of Respiratory Medicine,Luxian People's Hospital,Luzhou,Sichuan,646100,China)
出处
《黑龙江医学》
2026年第2期135-137,142,共4页
Heilongjiang Medical Journal
基金
四川省中医药管理局科学技术研究专项课题基金资助项目(2023MS158)。
关键词
哮喘
氧化应激
和厚朴酚
炎症
Asthma
Oxidative stress
Honokiol
Inflammation
