COPD营养不良大鼠下丘脑瘦素受体活化后STAT3、SOCS3的表达研究  

Expression of STAT3 and SOCS3 following leptin receptor activation in hypothalamus in COPD rats with malnutrition

作　　者：徐志波[1] 陈芳[2] 江劲[1] XU Zhibo;CHEN Fang;JIANG jin

机构地区：[1]浙江中医药大学附属第二医院呼吸内科,杭州310005 [2]浙江中医药大学附属第一医院肺功能室

出　　处：《浙江医学》2017年第5期358-361,共4页Zhejiang Medical Journal

基　　金：国家自然基金项目(2012R10063);浙江省卫生厅一般项目(2013KYA140);浙江省博士后科研资助项目(BSH1402070)

摘　　要：目的通过检测慢性阻塞性肺疾病(COPD)合并营养不良大鼠血清瘦素及其下丘脑受体活化后信号传导转录活化因子3(STAT3)、细胞因子信号传导抑制因子3(SOCS3)的表达,推测其在介导类似于恶病质的COPD营养不良出现的可能机制。方法将30只SD大鼠分为两组:正常组、COPD组各15只。两组大鼠在自制熏烟箱内被动吸烟24周,并在第30、45天于气道内滴入脂多糖(LPS)0.2ml。观察各组大鼠的一般情况,检测血清瘦素、TG、低密度脂蛋白(VLDL)水平,制作肺组织HE病理切片,Western-blot法测定下丘脑STAT3、SOCS3相对表达量。结果 COPD组大鼠肺细支气管管壁厚度、管壁面积、管壁面积/腔周长均较正常组增加,差异均有统计学意义(t=7.633、18.843、8.470,均P<0.01),COPD组体重、TG、VLDL、瘦素、SOCS3的表达均低于正常组,差异均有统计学意义(t=-8.199、-16.736、-4.043、-6.235、-8.738,均P<0.01),而STAT3表达水平则高于正常组(t=18.860,P<0.01)。结论 COPD大鼠合并营养不良的出现,可能与瘦素作用于下丘脑受体后引起信号转导分子STAT3表达上调和SOCS3表达下调有关。Objective To investigate the expression of STAT3and SOCS3following leptin receptor activation in hypothalamus in COPD rats with malnutrition state.Methods Thirty SD rats were randomly divided into control group and COPD group with15in each group.Rats in COPD group received passive smoking for24weeks,then LPS0.2ml was dripped in the airway at d30and d45.All animals were sacrificed after experiments;serum leptin,triglycerides,VLDL were measured;and pathological examination of lung tissue was performed;relative expression of STAT3and SOCS3in hypothalamus was detected by Western-Blot.Results The body weight,and triglycerides,VLDL,leptin levels,and the expression of SOCS3in COPD group were lower than those in normal group(all P<0.01),while the expression of STAT3was higher(P<0.01).Conclusion The malnutrition state in COPD rats may be related to the leptin-mediated up-regulation of STAT3expression and down-regulation of SOCS3expression in hyothalamus.

关 键 词：瘦素 慢性阻塞性肺疾病 营养不良 信号传导转录活化因子3 细胞因子信号传导抑制因子3 

分 类 号：R563.9[医药卫生—呼吸系统] R591[医药卫生—内科学]