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作 者:曾源[1] 杨威[1] 张小强[1] 李斌[1] 董啸[1]
机构地区:[1]南昌大学医学院第二附属医院心胸外科,江西南昌330006
出 处:《重庆医学》2013年第28期3388-3389,3392,共3页Chongqing medicine
基 金:国家自然科学基金资助项目(81260054)
摘 要:目的探讨前B细胞克隆增强因子(PBEF)在体外循环(CPB)术后肺血管内皮通透性增加中的机制,为提出更好的CPB期间肺保护措施提供依据。方法建立动物模型并进行分组,A组:大鼠行慢病毒AD-PBEFshRNA转染;B组:大鼠进行30min深低温停循环;C组:大鼠行慢病毒AD-PBEFshRNA转染后,再进行30min深低温停循环;对照组:大鼠只进行麻醉、CPB插管,不行CPB转流;应用Western blotting和酶联免疫吸附法检测各组大鼠肺组织PBEF的表达情况。结果 C组的PBEF、磷酸化P38MAPK、磷酸化ERK、磷酸化MLC、磷酸化VE-cadherin、磷酸化FAK表达与A、B组、对照组比较差异有统计学意义(P<0.05);C组VEGF、MMP2、MMP9、W/D与A、B组、对照组比较差异有统计学意义(P<0.05)。病理结果显示,对照组大鼠肺组织正常,C组肺组织病理损害严重,A、B组较C组有不同程度的减轻。结论 PBEF通过MAPK/PI3K-Akt/VEGF信号转导通路来增加CPB术后肺血管内皮通透性。Objective To investigate the mechanism of PBEF in pulmonary vascular endothelial permeability increasing after car- diopulmonory bypass,in order to provide the basis for a better lung protective measures during cardiopulmonary bypass. Methods Animal models were established, group A: the rats were transfected with the lentiviral AD-PBEFshRNA; group B: the rats were took 30 min deep hypothermic circulatory arrest ~ group C:the rats were took 30 rain deep hypothermic circulatory arrest, then trans- fected with the lentiviral AD-PBEFshRNA; control group:the rats were anesthetized and established CPB tube, without CPB by- pass. Lung tissue was detected with Western blotting and ELISA. Results PBEF,phosphorylation of P38MAPK, ERK, MLC, VE- cadherin, FAK in group C had significant difference with group A, B and the control group(P〈0.05). VEGF, MMP2, MMP9, W/D in group C had significant difference with group A, B and the control group(P〈0.05). The pathological results showed that rat lung tissue of the control group was normal, while in group C,it had severe pathological damage, the pathological damage degree in group A,B reduced compared to group C. Conclusion PBEF can through MAPK/PI3K-Akt/VEGF signaling pathway, increase pulmonary vascular endothelial permeability.
关 键 词:前B细胞克隆增强因子 体外循环 肺血管内皮 通透性
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