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作 者:汤涛 陈铜兵[1] 王辉[1] TANG Tao;CHEN Tongbing;WANG Hui(Department of Pathology,the First People’s Hospital of Changzhou,Jiangsu,Changzhou 213003,China)
机构地区:[1]江苏省常州市第一人民医院病理科,江苏常州213003
出 处:《中国医药科学》2022年第8期27-31,共5页China Medicine And Pharmacy
基 金:江苏省常州市卫健委青年人才科技项目(QN202005)。
摘 要:目的探讨去甲肾上腺素(NE)在百草枯中毒导致肺纤维化中的作用。方法选取苏州大学附属第三医院急诊科收治的41例百草枯中毒患者和6只实验小鼠的血浆,实验组和对照组小鼠各3只,实验组用百草枯处理,高效液相色谱电化学法检测血浆中NE浓度。采用微渗透泵构建小鼠模型,实验组9只,对照组小鼠3只,实验组用百草枯加NE处理,对照组仅用百草枯处理。模拟NE受体阻断剂普萘洛尔对百草枯中毒引起的肺纤维化模型,实验组和对照组小鼠各18只,实验组用百草枯加NE加普萘洛尔处理,对照组中普萘洛尔换成等量的乙醇。结果研究显示百草枯中毒患者的NE水平显著提高,而中毒实验小鼠NE并没有提高。体外细胞实验显示,NE在体外可诱导人肺泡Ⅱ型上皮细胞发生上皮间质转化,从而协同百草枯中毒致肺纤维化,小鼠实验发现实验组用NE处理的小鼠肺纤维化程度高于对照组。普萘洛尔实验显示,实验组加了普萘洛尔后百草枯中毒小鼠的肺纤维化程度明显低于对照组。结论NE可能是导致临床百草枯中毒致肺纤维化疗效不佳的重要原因,普萘洛尔在临床上对百草枯中毒所致的肺纤维化有一定的预防作用。Objective To investigate the effect of norepinephrine in pulmonary fibrosis induced by paraquat poisoning.Methods The plasma of 41 paraquat poisoning patients who were admitted to the emergency department of the Third Affiliated Hospital of Soochow University and plasma of 6 experimental mice were selected,with 3 mice each in the experimental group and the control group.The experimental group was treated with paraquat,and the high-performance liquid chromatography with electrochemical detection was used to determine the concentration of norepinephrine in plasma.A micro-osmotic pump was used to construct a mouse model,with 9 mice in the experimental group and 3 mice in the control group.The experimental group was treated with paraquat plus norepinephrine,and the control group was treated with paraquat only.A model of pulmonary fibrosis induced by paraquat poisoning with propranolol,a norepinephrine receptor blocker,was established.There were 18 mice in each of the experimental group and the control group.The experimental group was treated with paraquat plus norepinephrine plus propranolol,and propranolol in the control group was replaced with the same amount of ethanol.Results The study showed that the level of norepinephrine in paraquat poisoned patients was significantly increased,while it did not increase in poisoned experimental mice.In vitro cell experiments showed that norepinephrine induced epithelial-mesenchymal transition in human alveolar type Ⅱ epithelial cells in vitro,thereby cooperating with paraquat poisoning to induce pulmonary fibrosis.Experiments in mice found that the degree of pulmonary fibrosis in mice treated with norepinephrine in the experimental group was higher than that in the control group.The propranolol experiment showed that the degree of pulmonary fibrosis in the paraquat poisoned mice in the experimental group with addition of propranolol was significantly lower than that of the control group.Conclusion Norepinephrine may be an important reason for the poor efficacy of clinical p
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