虎杖苷对慢性阻塞性肺疾病大鼠PI3K/AKT/mTOR通路以及气道炎症的影响  

Effects of polydatin on PI3K/AKT/mTOR pathway and airway inflammation in rats with chronic obstructive pulmonary disease

作　　者：史方海 陈忠仁[1] SHI Fanghai;CHEN Zhongren(Department of respiratory medicine,Haikou People’s Hospital,Haikou 570208,China)

机构地区：[1]海口市人民医院呼吸内科,海南海口570208

出　　处：《药物评价研究》2020年第10期1983-1987,共5页Drug Evaluation Research

基　　金：海南省自然科学基金面上项目(818MS136)。

摘　　要：目的构建慢性阻塞性肺疾病(COPD)大鼠模型,探讨虎杖苷对COPD大鼠PI3K/AKT/mTOR通路以及气道炎症的影响。方法 100只Wistar大鼠随机分为对照组、模型组、地塞米松(0.2 mg/kg,阳性药)组和虎杖苷低、高剂量(30、60 mg/kg)组,每组20只。除对照组外,其他组熏香烟加气管注射内毒素法制备COPD模型,COPD造模前1 d开始ig给药,每天1次,持续30 d。ELISA法检测支气管肺泡灌洗液(BALF)中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6水平;RSE3020肺功能检测仪测定用力肺活量(FVC)、第1秒用力呼气容积(FEV1)、呼气峰流速(PEF);取肺组织4%甲醛固定后制作切片,HE染色,并进行肺组织损伤病理评分;Western blotting检测肺组织PI3K、AKT、mTOR蛋白表达。结果虎杖苷高、低剂量组大鼠BALF中TNF-α和IL-6表达水平、肺组织损伤病理评分以及PI3K、AKT和mTOR蛋白表达均显著低于模型组(P<0.01);虎杖苷高、低剂量组大鼠FVC、FEV1、PEF肺功能指标显著高于模型组(P<0.01)。结论虎杖苷可以抑制COPD大鼠PI3K/AKT/mTOR通路,抑制气道炎症,发挥肺损伤保护作用。Objective To observe the effects of polydatin on PI3 K/AKT/mTOR pathway and airway inflammation in rats with chronic obstructive pulmonary disease(COPD).Methods Totally 100 Wistar rats were devided into control group, model group,dexamethasone(0.2 mg/kg, positive drug) group and low and high dose of polydatin(30, 60 mg/kg) groups, with 20 rats in each group.Except for control group, the COPD models were prepared bypassive cigarette smoking and intratracheal.Ig administration was started one day before COPD modeling, once a day, lasting for 30 days.The expression of TNF-α and IL-6 in BALF was detected by ELISA analysis.The FVC, FEV1, and PEF was used to determined lung function.HE staining was used to determined pathological score of lung tissue injury(LDPS scores).Western blot was used to detect protein expression of PI3 K, AKT and mTOR in lung tissue.Results The expression of TNF-α and IL-6 in BALF, LDPS scores, expression of PI3 K, AKT, mTOR in low and high dose of polydatin group was significantly lower than that in COPD model group(P < 0.01) and the FVC, FEV1, and PEF was significantly higher than that in COPD model group(P < 0.01).Conclusion Polydatin can inhibit PI3 K/AKT/mTOR pathway to block airway inflammation in rats and protect lung destroy in COPD rats.

关 键 词：虎杖苷 慢性阻塞性肺疾病(COPD) PI3K/AKT/mTOR信号通路 气道炎症 大鼠 

分 类 号：R285.5[医药卫生—中药学]