番茄红素抗哮喘作用及机制研究

Effects and mechanism of Lycopene on anti-asthma

目的:探讨番茄红素对哮喘气道炎症的影响及可能的作用机制。方法:雄性BALB/c小鼠40只随机分为对照组(control)、模型组(model)、番茄红素低剂量组(LYC 50 mg/kg)和番茄红素高剂量组(LYC 100 mg/kg)。卵清蛋白诱导建立哮喘模型。收集支气管肺泡灌洗液(BALF),Diff-quik染色进行炎症细胞计数,HE染色观察肺组织病理学变化,ELISA和Western blot分别检测IL-4、IL-5和IL-13水平,乙酰甲胆碱雾化吸入检测哮喘小鼠气道高反应性,利用荧光探针DCFH-DA检测ROS水平,比色法检测SOD活性和MDA含量,Western blot法检测p-PI3K、p-AKT以及p-p65蛋白表达水平。结果:番茄红素能够明显降低哮喘小鼠BALF中炎症细胞数,改善哮喘小鼠肺组织病理改变及气道高反应性,降低哮喘小鼠BALF和肺组织中IL-4、IL-5和IL-13水平,降低ROS水平和MDA含量,提高SOD活性,抑制p-PI3K、p-AKT以及p-p65蛋白表达。结论:番茄红素通过抑制ROS调控的PI3K/AKT/NF-κB信号通路发挥抗哮喘作用。

Objective:To investigate the effect of lycopene on airway inflammation in asthma and its possible mechanism.Methods:Forty male BALB/c mice were randomly divided into control group,model group,lycopene low dose group(LYC 50 mg/kg)and lycopene high dose group(LYC 100 mg/kg).Ovalbumin(OVA)was injected intraperitoneally and inhaled to induce the asthmatic model.The numbers of total cells and classified cells in bronchoalveolar lavage fluid(BALF)were observed by diff-quik staining.HE staining was used to observe pathological changes of lung tissue.ELISA and Western blot were used to detect IL-4,IL-5 and IL-13 levels,and methacholine aerosol inhalation.Airway hyperresponsiveness of asthmatic mice was detected by inhalation of acetylcholine atomization.Fluorescence probe DCFH-DA was used to detect the level of reactive oxygen species.The activity of SOD and the content of MDA were detected by colorimetry.The expression levels of p-PI3K,p-AKT and p-p65 protein in lung tissue were determined by Western blot.Results:Lycopene significantly reduced the number of inflammatory cells in BALF of asthmatic mice,improved lung pathological changes and airway hyperresponsiveness in asthmatic mice,reduced IL-4,IL-5,and IL-13 levels in BALF and lung tissues of asthmatic mice,decreased ROS and MDA levels,increased SOD activity,and inhibited p-PI3K,p-AKT and p-p65 protein expression.Conclusion:Lycopene exerted anti-asthmatic effects by inhibiting ROS-regulated PI3K/AKT/NF-κB signaling pathway.