鱼腥草素钠对慢性阻塞性肺疾病模型大鼠肺组织PI3K、AKT1及mTOR mRNA表达的影响  

Effect of sodium houttuyfonate on the expression of PI3K,AKT1 and mTOR mRNA in the lung of rat models of chronic obstructive pulmonary disease

作　　者：吴中华[1] 闫玲玲[1] 杨爱东[1] 张海英[1] 符胜光[1] 杨云翔 WU Zhonghua;YAN Lingling;YANG Aidong;ZHANG Haiying;FU Shengguang;YANG Yunxiang(Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China;Shanghai WeiYu High School, Shanghai 200231)

机构地区：[1]上海中医药大学,上海201203 [2]上海市位育中学,上海200231

出　　处：《中国实验动物学报》2018年第1期8-12,共5页Acta Laboratorium Animalis Scientia Sinica

基　　金：国家自然科学基金面上项目(No.81673855);上海中医药大学学科能力提升项目~~

摘　　要：目的观察鱼腥草素钠对慢性阻塞性肺疾病模型大鼠肺组织中PI3K、AKT1及mTOR mRNA表达的影响,并探讨其作用机制。方法选取Wistar雄性大鼠24只,体重(220±20)g,随机分为正常组、模型组、地塞米松组和鱼腥草素钠组(每组6只)。采用烟熏和脂多糖气管滴注联合方法建立慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)大鼠模型,采用实时荧光定量聚合酶链反应检测PI3K、AKT1及mTOR mRNA表达,并观察大鼠肺组织病理变化。结果与正常组相比,模型组大鼠肺组织PI3K、AKT1 mRNA表达显著增高(P<0.01,P<0.05),mTOR mRNA表达显著降低(P<0.01);与模型组相比,鱼腥草素钠组和地塞米松组肺组织PI3K、AKT1 mRNA表达显著降低(P<0.01,P<0.05),mTOR mRNA表达显著增高(P<0.01);与地塞米松组相比,鱼腥草素钠组肺组织mTOR mRNA表达显著增高(P<0.05)。病理观察结果显示,与正常组比较,模型组局部肺实变,肺泡腔内大量中性粒细胞浸润,胶原染色显示肺间质纤维组织大量增生;鱼腥草素钠组和地塞米松组肺组织病理改变明显轻于模型组,鱼腥草素钠组和地塞米松组肺组织呈轻度间质性肺炎,仅见少量的纤维组织增生。结论鱼腥草素钠能够减轻慢性阻塞性肺疾病模型大鼠肺组织损伤,其机制可能与其能够下调PI3K、AKT1 mRNA的表达、上调mTORmRNA表达有关。Objective To investigate the effect of sodium houttuyfonate on the expression of PI3K and AKT1 and mTOR mRNA in the lung of rats with chronic obstructive pulmonary disease（ COPD）,and reveal the possible mechanism of the COPD treated with sodium houttuyfonate. Methods Twenty-four male Wistar rats were randomly divided into normal control group,model control group,dexamethasone group and sodium houttuyfonate group（ n = 6 for each）. The rat models of COPD were established by intratracheal instillation of lipopolysaccharide and smudging. The expressions of PI3K and AKT1 and mTOR mRNA were determined by real-time PCR. The morphological changes of the lung tissue was examined by histopathology. Results Compared with the normal control group,the expressions of PI3K and AKT1 were significantly increased and mTOR mRNA was significantly decreased in the model group（ P〈0. 01,P〈0. 05）. Compared with the model group,the expressions of PI3K and AKT1 were significantly decreased and mTOR mRNA was significantly increased in the sodium houttuyfonate group and dexamethasone group（ P〈0. 01,P〈0. 05）. Compared with the dexamethasone group,the expression of mTOR mRNA was significantly increased in the sodium houttuyfonate group（ P〈0. 05）. The pathological observation indicated that there were local pulmonary consolidation and a extensive neutrophil infiltration in the alveolar cavity. Prominent pulmonary interstitial fibrous hyperplasia was observed in the model group. The pathological manifestations were much ameliorated than those of the model group,and only mild interstitial pneumonia and a slight fibrous hyperplasia were seen in the sodium houttuyfonate and the dexamethasone groups. Conclusions Sodium houttuyfonate reduces the injury of lung tissue and has protective effect on COPD rats. The mechanism is probably related to the down-regulatation of expression of PI3K and AKT1 mRNA and up-regulatation of expression of mTOR mRNA in COPD rats.

关 键 词：鱼腥草素钠 慢性阻塞性肺疾病 磷脂酰肌醇3激酶 丝氨酸苏氨酸蛋白激酶 雷帕霉素靶蛋白 大鼠 

分 类 号：Q95-33[生物学—动物学]