摘要
目的:探讨保肺定喘汤对COPD大鼠瘦素及下丘脑瘦素受体活化后信号通路JAK2/STAT3的影响。方法将40只SD大鼠随机分为4组:正常组、保肺定喘汤预防组、保肺定喘汤治疗组和COPD组,每组各10只。除正常组外,各组大鼠在自制熏烟箱内被动吸烟24周,并在第30天和第45天于气道内滴入脂多糖(LPS)。观察各组大鼠的一般情况,检测血清瘦素水平,肺组织HE染色,Western-Blot法测定下丘脑STAT3、PIAS3、SOCS3相对表达量。结果保肺定喘汤预防组与治疗组大鼠体重、血清瘦素水平均明显高于COPD组(P〈0.05、P〈0.01)。保肺定喘汤预防组与治疗组STAT3、PIAS3均低于COPD组(P均〈0.01);保肺定喘汤预防组与治疗组SOCS3高于COPD组,差异均有统计学意义(P〈0.05),且两组SOCS3相对表达量与正常组比较差异有显著性(P〈0.01)。结论保肺定喘汤能够减轻长期吸烟导致的COPD大鼠气道重塑,增加体重,提高血清瘦素水平,其机理与下丘脑信号通路JAK2/STAT3相关,使STAT3、PIAS3表达上调,SOCS3表达下调。
Objective To discuss the treatment effect of Baofei Dingchuan decoction on leptin and hypothalamus JAK2/STAT3 pathway in COPD rat model. Method 40 SD mices are randomly divided into normal group, prevention and treatment group of Baofei Dingchuan decoction and COPD group, each group have 10 SD rats. In addition to the normal group, each group of rats were explored smoking in homemade box during the 24 weeks. At the time of 30 and 45 days, each mice of prevention and treatment group of Baofei Dingchuan decoction and COPD group are dripped LPS into its airway. Prevention group were given Baodei Dingchuan decoction at the beginning of Passive smoking. While treatment group were given at the end of 4 weeks. At last, all the rats were executed and detected their serum leptin. Pathological examination on lung tissue, and determination relative expression of hypothalamus STAT3、PIAS3、SOCS3 by Western-Blot method. Results Rats of prevention and treatment groups were higher than the COPD group (P〈0.05, P〈0.01) in weight and leptin level. The expression of STAT3, PIAS3 in Prevention and treatment groups were lower than the COPD group (P〈0.01). The SOCS3 levels of prevention and treatment groups were higher than COPD group (P〈0.05) .Compared with normal group, there are significant differences (P〈0.01). Conclusion Baofei Dingchuan decoction can alleviate the airway remodeling and increase the weight in long-term smoking induced COPD rats model. The level of serum leptin also improved by the treatment of Baofei Dingchuan decoction. The mechanism might associated with the hypothalamus JAK2/STAT3 pathway. It can up-regulate the expression of STAT3, PIAS3 and down-regulate the expression of SOCS3 in COPD rat models.
出处
《浙江临床医学》
2015年第4期525-527,共3页
Zhejiang Clinical Medical Journal
基金
国家自然科学基金项目(2012R10063)
浙江省中医药管理局项目(2011ZQ009)
浙江省卫生厅项目(2013KYA140)