利金方对慢性阻塞性肺疾病大鼠模型JAK2-STAT3-RORyt信号通路的影响  

Effect of Lijin Recipe on JAK2-STAT3-RORYT Signaling Pathway in Chronic Obstructive Pulmonary Disease Rat Model

作　　者：陈斯宁[1] 李瑞祥[1] 黎展华 黄文锋 冯玉青[3] 王浩舟[1] CHEN Si-ning;LI Rui-xiang;LI Zhan-hua;HUANG Wen-feng;FENG Yu-qing;WANG Hao-zhou(Department of Respiratory Medicine,Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine,Nanning(530001);Department of Intensive Care,Qingyuan City Hospital of Traditional Chinese Medicine,Guangdong(511500);Department of Clinical Laboratory,Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine,Nanning(530001))

机构地区：[1]广西中医药大学附属瑞康医院呼吸内科,南宁530001 [2]广东省清远市中医院重症医学科,广东511500 [3]广西中医药大学附属瑞康医院检验科,南宁530001

出　　处：《中国中西医结合杂志》2022年第1期89-95,共7页Chinese Journal of Integrated Traditional and Western Medicine

基　　金：国家自然科学基金资助项目(No.81760853)。

摘　　要：目的探讨利金方对慢性阻塞性肺疾病(COPD)大鼠炎症细胞抑制作用的影响。方法将105只SPF级Wistar大鼠随机分为7组:空白组、模型组、利金方低剂量组、利金方中剂量组、利金方高剂量组、JAK2抑制剂组、STAT3抑制剂组,每组15只。除空白组外,其余各组通过烟熏等复合因素建立COPD大鼠模型。造模结束后,空白组、模型组给予生理盐水灌胃,利金方低剂量(3 g/mL)组、利金方中剂量(10.5 g/mL)组、利金方高剂量(21 g/mL)组分别给予不同浓度利金方灌胃,JAK2抑制剂组、STAT3抑制剂组分别予酪氨酸磷酸化抑制剂(AG490)试剂和STAT3信号传导通路抑制剂(WP1193)试剂腹腔注射。给药7天后,分别检测大鼠肺组织中JAK2、STAT3、p-STAT3、RORyt蛋白表达,肺组织中JAK2、STAT3、RORyt mRNA表达以及大鼠血清与支气管肺泡灌洗液(BALF)中IL-17含量。结果与空白组比较,模型组肺组织中JAK2、STAT3、p-STAT3、RORyt蛋白表达与肺组织中JAK2、STAT3、RORyt mRNA表达,及血清与BALF中IL-17分泌均升高(P<0.05);与模型组比较,用药组大鼠肺组织中JAK2、STAT3、p-STAT3、RORyt蛋白表达和肺组织JAK2、STAT3、RORyt mRNA表达以及大鼠血清、BALF中IL-17含量均下降(P<0.05,P<0.01);与利金方低剂量组比较,利金方高剂量组大鼠肺组织中JAK2、STAT3、p-STAT3、RORyt蛋白表达和肺组织JAK2、STAT3、RORyt mRNA表达以及大鼠血清、BALF中IL-17含量均下降(P<0.01);与利金方中剂量组比较,利金方高剂量组大鼠肺组织中JAK2、STAT3、p-STAT3、RORyt蛋白表达和肺组织JAK2、STAT3、RORyt mRNA表达以及大鼠血清、BALF中IL-17含量均下降(P<0.01)。结论利金方能够通过调控细胞免疫中上游JAK2-STAT3-RORyt信号通路,抑制炎症细胞分泌从而起到抗免疫炎症作用。Objective To observe the effect of Lijin Recipe(LJR) on the inhibition of inflammatory cells in chronic obstructive pulmonary disease(COPD) rats. Methods A total of 105 SPF Wistar rats were randomly divided into 7 groups: blank group, model group, low, medium, high dose LJR groups, JAK2 inhibitor group, and STAT3 inhibitor group, 15 rats in each group. Except blank group,COPD rat model was established in the other groups by smoking and other compound factors. After modeling rats in blank group and model group were intragastrically given normal saline. Rats in each LJR groups were intragastrically given different concentrations of LJR(3,10.5, 21 g/mL, respectively). JAK2 inhibitor group and STAT3 inhibitor group were intraperitoneally injected with tyrosine phosphorylation inhibitor(AG490) reagent and STAT3 signaling pathway inhibitor(WP1193) reagent respectively. After 7 days of administration, protein expressions of JAK2, STAT3, p-STAT3, and RORYT in lung tissue, mRNA expressions of JAK2, STAT3, and RORYT in lung tissue, and the IL-17 content in serum and bronchoalveolar lavage fluid(BALF) of rats were detected. Results Compared with the blank group, protein expressions of JAK2, STAT3, p-STAT3, and RORyT in lung tissues, mRNA expressions of JAK2, STAT3, and RORYT in lung tissues, IL-17 secretion in serum and BALF increased(all P<0.05) in the model group.Compared with the model group, protein expressions of JAK2, STAT3, p-STAT3, and RORyT in lung tissue, and mRNA expressions of JAK2, STAT3, and RORyT in lung tissue, the content of IL-17 in BALF and serum decreased in each treatment group(P<0.05, P<0.01). Compared with low dose LJR group, protein expressions of JAK2,STAT3, p-STAT3, and RORyT, mRNA expressions of JAK2, STAT3, and RORyT in lung tissues, and the content of IL-17 in serum and BALF decreased in high dose LJR group(all P<0.01). Compared with the medium dose LJR group, protein expressions of JAK2, STAT3, p-STAT3, and RORyT, mRNA expressions of JAK2, STAT3, and RORyT in lung tissue, and the content of IL-

关 键 词：慢性阻塞性肺疾病 利金方 JAK2 STAT3 RORyt 信号通路 中药 

分 类 号：R285.5[医药卫生—中药学]