秦皮甙对重症肺炎大鼠炎症因子表达及相关通路活化的影响  

Effects of Fraxin on inflammatory factors expression and related pathways activation of rats with severe pneumonia

作　　者：吴萍 何文龙[1] 付云[1] 吴杰 李健羽 肖丽 WU Ping;HE Wenlong;FU Yun;WU Jie;LI Jianyu;XIAO Li(Department of Critical Medicine,Xinxiang Central Hospital,Xinxiang 453000,China;Department of Critical Medicine,First Affiliated Hospital of Xinxiang Medical College,Xinxiang 453000,China)

机构地区：[1]新乡市中心医院重症医学科,新乡453000 [2]新乡医学院第一附属医院重症医学科,新乡453000

出　　处：《免疫学杂志》2020年第4期292-298,共7页Immunological Journal

基　　金：河南省科技攻关计划(192102310332)。

摘　　要：目的研究研究秦皮甙(Fraxin)对肺炎克雷伯菌所致重症肺炎大鼠免疫功能及Janus蛋白酪氨酸激酶/信号转导和转录激活因子(JAK/STAT)和核转录因子κB(NF-κB)活化的作用。方法将50只雄性SD大鼠随机分为对照组,模型组和秦皮甙10、20和40 mg·kg^-1治疗组,通过肺炎克雷伯菌构建重症肺炎模型大鼠,秦皮甙灌胃干预治疗14 d后,组织观察和W/D比值分析肺组织损伤;采用HE染色进行病理学分析;ELISA试剂盒法检测各组大鼠血清中炎症因子IL-1β、IL-6、IL-10和IL-4的含量;Western blot印迹分析肺组织中活化的胱天蛋白酶3/9、JAK2/p-JAK2、STAT3/p-STAT3和P65/p-P65蛋白表达水平。结果与模型组比较,随着秦皮甙干预治疗剂量的增加,大鼠肺组织损伤评分和W/D值明显降低(P<0.05),肺损伤程度明显改善;肺组织中胱天蛋白酶3/9、p-JAK2、p-STST3和p-P65表达水平及血清中促炎症因子IL-1β和IL-6水平显著降低,抗炎因子IL-4和IL-10水平显著升高,差异均有统计学意义(P<0.05)。结论秦皮甙通过抑制JAK/STAT和激活NF-κB信号途径,抑制细胞凋亡,促进肺组织损伤修复,进而缓解肺炎克雷伯菌所致重症肺炎症状。To study the effect of Fraxin on the immune function and the activation of Janus protein tyrosine kinase/Signal transducer,transcription activator(JAK/STAT)and nuclear factorκB(NF-κB)in rats with severe pneumonia caused by Klebsiella pneumoniae,50 male SD rats were recruited and randomly divided into control group,model group,Fraxin 10,20 and 40 mg·kg^-1 groups.The model of rats with severe pneumonia was constructed with Klebsiella pneumoniae.Rats in Farxmin group were intervened with intragastric administration of Fraxin for14 d,and then the lung tissue damage was analyzed by tissue observation and W/D analysis.HE staining was applied for pathological analysis;ELISA Kit method was used to detect the contents of serum inflammatory factors such as IL-1β,IL-6,IL-10 and IL-4 of all the groups.Western blot was applied to analyze the expression levels of activated Caspase3/9,JAK2/p-JAK2,STAT3/p-STAT3 and P65/p-P65 proteins in lung tissues.Data showed that Fraxin intervention could improve the damaged lungs in a dose-dependent manner,resulting in lower lung tissue damage score and W/D of rats(P<0.05),as compared with model group.Furthermore,the expression levels of Caspase-3/9,p-JAK2,p-STST3 and p-P65 in lung tissues,and levels of pro-inflammatory factors IL-1βand IL-6 in serum were significantly decreased,while anti-inflammatory factors IL-4 and IL-10 levels were significantly increased(P<0.05)in Fraxin groups.Taken together,Fraxin inhibits apoptosis and promotes repair of lung tissue damage by inhibiting JAK/STAT and activating NF-κB signal pathway,thus relieving severe pneumonia symptoms caused by Klebsiella pneumoniae.

关 键 词：秦皮甙 重症肺炎 免疫功能 JAK/STAT NF-ΚB活化 

分 类 号：R563.1[医药卫生—呼吸系统]