染料木素对哮喘小鼠气道炎症及肺组织蛋白酪氨酸激酶JAK1表达的影响

摘要

Objective To explore the effect of genistein of fructus sophorae on airway inflammation and the expression of protein tyro-sine kinase Janus kinase 1(kinase Janus 1,JAK1) in mice with asthma. Methods Thirty-two BALB/c female mice were randomly divided into control group(n=10), asthma model group(n=11) and genistein group(n=11). The mice in model group and genistein group were sensitized and excited with ovalbumin( OVA) to establish the model of asthma, while the mice in control group were given the same amount of normal saline instead of OVA at the same time. The mice in genistein group were intraperitoneally injected with 30 mg/kg genistein 30 min before atomization inhalation. The expression of JAK1 in lung tissues was detected by Western blot. The patho-logical changes of airway inflammation in mice were observed under light microscope by HE staining. Results The expression of JAK1 in lung tissues were significantly higher in model group than in control group(P<0. 01). The expression of JAK1 in lung tissues was significantly lower in genistein group than in model group(P<0. 01). In model group and genistein group, the pathological scores were (9. 697 ± 1. 768)and (5. 000 ± 2. 620)respectively, and both were significantly higher than in control group(0. 198 ± 0. 170)(P<0. 01). In control group, there was no inflammatory cell infiltration around the bronchus and blood vessels. In genistein group, there were a small amount of lymphocytes accompanied with neutrophils infiltration around the bronchus and blood vessels. In model group, there were a large number of lymphocytes with neutrophils infiltration around the bronchus and blood vessel, and the bronchial epitheli-ums of some mice were shed, and there were a small amount of severe mucus secretion. Conclusion Genistein can down regulate the expression of protein tyrosine kinase JAK1, and alleviate the airway inflammation in mice with asthma.%目的：探讨槐角染料木素对小鼠气道炎症及肺组织蛋白酪氨酸激酶Janus激酶1(Janus kinase 1,JAK1)的影响。方法32只雌性BALB/c小鼠随机分为对照组(n=10)、哮喘模型组(n=11)和染料木素干预组(n=11)。模型组和干预组采用卵清蛋白( OVA)腹腔注射致敏和雾化吸入激发,建立哮喘小鼠模型。对照组于相同时间采用等量生理盐水代替OVA。干预组于雾化吸入前30 min给予染料木素30 mg/kg腹腔注射。用免疫印迹法观察小鼠肺组织中JAK1的表达。制作肺组织病理切片,HE染色后光镜下观察小鼠气道炎症的病理学变化。结果模型组小鼠肺组织中JAK1的表达水平明显高于对照组(P<0.01)；干预组小鼠肺组织中JAK1的表达水平明显低于模型组(P<0.01)。模型组和干预组小鼠肺组织炎症病理学评分分别是(9.697±1.768)分和(5.000±2.620)分,均明显高于对照组(0.198±0.170)分(均P<0.01)；干预组小鼠肺组织炎症病理学评分明显低于模型组(P<0.01)。病理切片观察结果示,对照组支气管及血管周围无炎性细胞浸润；干预组小鼠支气管和血管周围有少量淋巴细胞伴随中性粒细胞浸润；模型组支气管和血管周围有大量淋巴细胞及中性粒细胞浸润,部分小鼠支气管上皮脱落,少量出现严重的黏液分泌。结论染料木素可下调哮喘小鼠蛋白酪氨酸激酶JAK1的表达,减轻哮喘小鼠气道炎症反应,可能是其缓解哮喘的作用机制。