为探讨紫菀酮对卵清蛋白(ovalbumin, OVA)诱导哮喘幼鼠的作用及相关机制，将幼鼠随机分成正常对照组、哮喘模型组、紫菀酮组和地塞米松组。除正常对照组外，其余各组采用OVA构建哮喘模型，紫菀酮组按照80 mg/kg的剂量灌胃给药，地塞米松组雾化吸入剂量为10.5 mg/kg。收集小鼠肺泡灌洗液(bronchoalveolar lavage fluid, BALF)进行细胞分类计数，原位末端转移酶标记 (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, TUNEL)染色观察肺组织中细胞凋亡损伤，生化法检测血清及肺组织中超氧化物歧化酶(superoxide dismutase, SOD)、丙二醛(malondialdehyde, MDA)和一氧化氮(nitric oxide, NO)水平，流式细胞术检测肺组织活性氧类(reactive oxygen species, ROS)含量，Western blotting检测肺组织中NF-κB及其磷酸化蛋白的表达水平。结果显示，OVA刺激后幼鼠出现呼吸加快、打喷嚏、口鼻发紫等哮喘症状。与模型组比较，紫菀酮组和地塞米松组幼鼠BALF中总细胞数、嗜酸性粒细胞数均显著减少(均P＜0.05)，中性粒细胞和巨噬细胞数显著增加(均P＜0.05)。紫菀酮组和地塞米松组幼鼠肺组织中细胞凋亡损伤减少，SOD含量增加(均P＜0.05)，MDA和NO含量显著降低(均P＜0.05)，ROS水平均显著降低(均P＜0.05)，p-NF-κB蛋白表达水平显著降低(均P＜0.05)，紫菀酮组与地塞米松组两两比较治疗效果无显著差异(均P＞0.05)。由此，紫菀酮能有效缓解哮喘症状，减少肺组织细胞凋亡损伤和炎症细胞浸润，其作用机制可能与抑制氧化应激和NF-κB信号通路有关，紫菀酮治疗支气管哮喘的药理作用与地塞米松类似。

This study aimed to explore the therapeutic effect and mechanism of shionone in ovalbumin (OVA) -induced asthma. For this purpose, asthma models were established in immature rats and the rats were randomly divided into the control group, asthma model group, shionone treatment group, and dexamethasone treatment group. Except for the control group, OVA was used to construct asthma model. The shionone group was administered with a dose of 80 mg/kg by gavaging, and the dexamethasone group was given aerosol inhalation at a dose of 10.5 mg/kg. Next, the bronchoalveolar lavage fluid (BALF) was collected and cells were counted. Cell apoptosis was observed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining in lung tissue. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and nitric oxide (NO) in serum and lung tissue were determined by biochemical methods. The levels of reactive oxygen species (ROS) in lung tissue were determined by flow cytometry. The expression levels of NF-κB and p-NF-κB in lung tissues were detected by Western blotting. After OVA stimulation, asthma symptoms such as accelerated breathing, sneezing, and purple nose and mouth were observed. Compared to the model group, the total number of cells and eosinophils number in the BALF of shionone group and dexamethasone group were significantly decreased (all P＜0.05), while the number of macrophages and neutrophils were increased (all P＜0.05). The cell apoptosis in lung tissues was decreased in shionone and dexamethasone group; the activity of SOD increased and the content of MDA and NO decreased significantly (all P＜0.05). The ROS level was significantly decreased (all P＜0.05). The protein expression level of p-NF-κB was significantly decreased (all P＜0.05). There was no significant difference in the therapeutic effect between the shionone group and the dexamethasone group (all P＞0.05). In conclusion, shionone can effectively relieve asthma symptoms, and reduce cell apoptosis and inflammatory cell infiltration in lung tissue. All these effects may be related to the inhibition of oxidative stress and NF-κB pathway. The pharmacodynamics of shionone in treating bronchial asthma is similar to dexamethasone.