机构地区:[1]中国中医科学院西苑医院心血管病中心,北京100091 [2]北京中医药大学东方医院,北京100078
出 处:《科学通报》2014年第12期1133-1139,共7页Chinese Science Bulletin
基 金:科技部国际科技合作与交流项目(2010DFA31690);国家自然科学基金(81273933);"十一五"国家科技攻关项目(2006BAI04A01)资助
摘 要:采用结扎左冠状动脉前降支制备实验性急性心肌梗死(acute myocardial infarction,AMI)模型大鼠,灌胃氯吡格雷和阿司匹林(双联抗)以及西洋参茎叶总皂苷(panax quinquefolius saponin,PQS),观察PQS在双联抗治疗过程中对大鼠胃黏膜损伤的修复作用.将实验性AMI模型手术成功的SD(Spragu-Dawley)大鼠随机分为AMI模型组、双抗组和双抗加PQS组,每组12只,另选12只大鼠作为假手术组(只穿线不结扎冠状动脉).各组动物造模后第2天开始灌胃,连续28 d后检测血清胃泌素(serum gastrin,GAS)、一氧化氮(nitric oxide,NO)、白细胞介素-1β(interleukin-1 beta,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor alpha,TNF-α)和血浆胃动素(motilin,MTL)、内皮素(endothelin-1,ET-1)的含量,观察胃黏膜组织病理和超微结构的变化.结果表明,与AMI模型组比较,双抗组大鼠胃黏膜Guth评分和Whittle评分显著升高(P<0.01).与双抗组比较,双抗加PQS组Guth评分和Whittle评分显著下降(P<0.01).与AMI模型组比较,双抗组大鼠血浆MTL、血清IL-1β及TNF-α含量显著升高(P<0.05),ET-1和GAS含量显著下降(P<0.05).与双抗组比较,双抗加PQS组大鼠的血清NO和GAS显著升高(P<0.05),血浆ET-1,MTL,血清IL-1β,TNF-α显著降低(P<0.05).PQS对双抗致大鼠胃黏膜的损伤具有一定的修复作用,其机理可能与促进GAS,NO保护因子的生成,减少炎性因子的分泌,降低ET-1,MTL损害因子水平等机制相关.We sought to evaluate the reparative effects of panax quinquefolius saponin (PQS) on gastric mucosal lesions induced by dual antiplatelet drugs. Sprague-Dawley (SD) rats (n=36) were randomly divided into two groups (n=12), the acute myocardial infarction (AMI) model group and the dual antiplatelet plus PQS group. The other 12 rats served as sham-operated controls. Infusing the rats after modelling for 28 days, we evaluated several factors. Blood plasma was collected to measure the content of serum gastrin (GAS), nitric oxide (NO), interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNFα), plasma motilin (MTL), and endothelin-1 (ET-1). We observed changes in histology and gastric mucosa ultrastructure. Compared with the AMI group, the gastric mucosa Guth and Whittle scores of the dual antiplatelet group increased significantly (P〈0.01). Compared with the dual antiplatelet group, the Guth and White scores of the dual antiplatelet plus PQS group significantly decreased (P〈0.01). Interestingly, the plasma MTL, serum IL-1β, and TNFα levels in the dual antiplatelet group improved compared with the AMI group (P〈0.05). However, ET-1 and GAS levels were reduced (P〈0.05). Compared with the dual antiplatelet group, the serum NO and GAS levels in the dual antiplatelet plus PQS group significantly increased (P〈0.05), and the plasma ET-1, MTL, serum IL-1β, and TNFα levels were reduced (P〈0.05). These results suggest that PQS has a certain reparative effect on gastric mucosa damage induced by dual antiplatelet drugs. The mechanism by which this occurs may be related to the promotion of GAS and NO protective factor formation, reduction of IL-1β and TNFα inflammatory factors, or the secretion of ET-1 and formation of MTL damage factors.
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