摘要
目的 探讨苦杏仁苷对卵白蛋白(OVA)诱导的哮喘小鼠Th1/Th2免疫失衡的作用及可能机制。方法 将40只BALB/c小鼠随机分为空白组、模型组、地塞米松组、苦杏仁苷组(15mg/kg),每组10只。通过OVA诱导小鼠模型,并使用药物连续治疗7天。治疗后进行取材,通过苏木精-伊红(HE)染色观察小鼠肺组织形态,通过ELISA法检测小鼠肺泡灌洗液(BALF)中胸腺基质淋巴细胞生成素(TSLP)、白细胞介素(IL-4)和干扰素-γ(IFN-γ)水平,通过Western blot法检测小鼠肺组织OX40配体(OX40L)、转录因子T-bet和GATA-3蛋白表达。结果 与模型组比较,地塞米松和苦杏仁苷组的一般情况明显改善,肺组织病理改变明显减轻,BALF中TSLP、IL-4显著降低(P<0.05),IFN-γ水平显著升高(P<0.05),小鼠肺组织中OX40L和GATA-3的蛋白表达水平均显著降低(P<0.05),T-bet蛋白表达水平均显著升高(P<0.05)。结论 苦杏仁苷对OVA诱导的哮喘小鼠具有良好的治疗作用,可能通过TSLP-DC-OX40L通路调节哮喘小鼠Th1/Th2免疫失衡,从而发挥治疗作用。
Objective To investigate the effect and possible mechanism of amygdaline on Th1/Th2 immune imbalance in egg albumin(OVA) in asthmatic mice.Methods 40 bablc mice were randomly divided into four groups,including control group,model group,dexamethasone group,and bitter almond group(15 mg/kg),and 10 mice per group.A mouse model was induced by OVA and treated with drugs for 7 consecutive days.After treatment,materials were taken and mouse lung tissue morphology was visualized by hematoxylin-eosin(HE) staining,and TSLP,IL-4 and IFN-γ levels in mouse BALF by ELISA assay of OX40 L,T-bet expression and GATA-3 in mouse lung tissues.Results Compared with the model group,dexamethasone and bitter amygdine groups improved generally and lung The pathological changes of lung tissue were alleviated.Compared with the model group,TSLP,IL-4 and IFN levels were significantly reduced in BALF in dexamethasone and bitter amygdine groups(P<0.05),and the protein expression levels of OX40 L,T-bet and GATA-3 were significantly reduced in mouse lung tissues(P<0.05).Conclusion Amygdalin has a good therapeutic effect on OVA-induced asthma in mice and bitter amygdine may modulate Th1/Th2 immune imbalance in asthmatic mice through the TSLP-DC-OX40 L pathway,thus exerting a therapeutic role.
作者
周欢
薛征
刘亚尊
崔雯
韩兆鹏
王雅娟
沈世平
ZHOU Huan;XUE Zheng;LIU Yazun(Affiliated Municipal Hospital of Traditional Chinese Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 200071,China)
出处
《医学研究杂志》
2022年第7期31-35,40,共6页
Journal of Medical Research
基金
国家自然科学基金资助项目(面上项目)(82074488)。
