芍药苷对哮喘小鼠炎症的作用及其机制研究

Effect of paeoniflorin on inflammation in asthmatic mice and its mechanism

目的:探讨芍药苷(PF)治疗哮喘小鼠炎症的作用及其可能机制。方法:将40只BALB/C雌性小鼠,随机分为5组:空白组、模型组、地塞米松组(阳性对照,2 mg/kg)、PF低剂量组(20 mg/kg)和PF高剂量组(40 mg/kg),采用卵清蛋白制备小鼠哮喘模型。测定小鼠肺泡灌洗液(BALF)中炎症细胞、炎症因子和活性氧(ROS)的含量,并检测肺组织中硫氧还蛋白/硫氧还蛋白反应蛋白(TXNIP)、Nod样受体蛋白3(NLRP3)、半胱氨酸天冬氨酸特异蛋白酶1(Caspase-1)mRNA的表达。结果:PF可显著降低哮喘小鼠BALF中白细胞、中性粒细胞、淋巴细胞和单核-巨噬细胞、ROS、IL-1β、IL-6和TNF-α的表达,缓解哮喘小鼠肺组织炎性细胞浸润,并降低哮喘小鼠肺组织中TXNIP、NLRP3和Caspase-1 mRNA的表达。结论:PF可改善哮喘小鼠的炎症反应,可能与其抑制ROS/TXNIP/NLRP3/Caspase-1信号通路有关。

Objective:To investigate the effect of paeoniflorin(PF)on inflammation in asthmatic mice and its possible mechanism.Methods:40 BALB/C female mice were randomly divided into five groups:blank group,model group,dexamethasone group(positive control,2 mg/kg),low dose PF group(20 mg/kg)and high dose PF group(40 mg/kg).Mouse asthma model is prepared with ovalbumin.The contents of inflammatory cells,inflammatory factors and reactive oxygen species(ROS)in BALF of mice were measured,and the expression of thioredoxin/thioredoxin reactive protein(TXNIP),Nod-like receptor protein3(NLRP3)and caspase-1(Caspase-1)mRNA in lung tissue were detected.Results:PF significantly decreased the expression of leukocyte,neutrophil,lymphocyte and monocyte-macrophage,ROS,IL-1β,IL-6 and TNF-αin BALF of asthmatic mice,relieved the inflammatory cell infiltration in the lung of asthmatic mice,and decreased the expression of TXNIP,NLRP3 and Caspase-1 mRNA in the lung of asthmatic mice.Conclusion:PF can improve the inflammatory response in asthmatic mice,which may be related to its inhibition of ROS/TXNIP/NLRP3/Caspase-1 signal pathway.