中文摘要：

目的：研究内皮-单核细胞激活多肽（ EMAP-Ⅱ）对体外血肿瘤屏障（ BTB）通透性的影响及可能机制。方法建立体外BTB模型, EMAP-Ⅱ处理后, millipore电阻测量系统检测跨内皮细胞阻抗（ TEER）值,采用Western blot方法检测pLKB1/LKB1、pAMPK/MAPK 和 p-mTORC1/ mTORC1的蛋白表达水平；分别应用LKB1抑制剂radicicol、AMPK抑制剂compound C和mTORC1激活剂IGF1进行预处理后再给予EMAPⅡ,检测体外BTB模型的TEER值,Western blot方法检测紧密连接相关蛋白ZO-1和occludin的蛋白表达水平。结果与 EMAP-Ⅱ0 h组相比, EMAP-Ⅱ可明显降低体外BTB 模型的 TEER 值,增加 p-LKB1/ LKB1和 p-AMPK/AMPK的表达水平,降低 p-mTORC1/mTORC1的表达水平,以上指标在EMAP-Ⅱ作用1 h时效果最明显；radicicol、com-pound C和IGF1预处理能够部分阻断EMAP-Ⅱ的作用,使体外BTB模型的TEER值及紧密连接相关蛋白ZO-1和occlu-din的表达水平明显增加。结论 EMAP-Ⅱ能明显增加体外BTB模型通透性,其机制可能与激活LKB1/AMPK/mTOR信号通路相关。

英文摘要：

Aim To investigate the effects of Endothe-lial-monocyte-activating polypeptide Ⅱ （ EMAP-Ⅱ） on the permeability of BTB model in vitro and the pos-sible mechanisms. Methods The BTB model in vitro was established and treated with EMAP-Ⅱ. After that, millipore resistance measurement system was used to detect the transendothelial resistance （ TEER ） value. The expressing levels of pLKB1/LKB1,pAMPK/MAPK and p-mTORC1/ mTORC1 were assessed by Western blot assay. After pretreatment with LKB1 inhibitor radicicol, AMPK inhibitor compound C and mTORC1 activator IGF 1 respectively , the BTB model in vitro was treated with EMAPⅡ. The TEER value of BTB model was detected. Western blot assay was used to measure the expressing levels of tight junction associated protein ZO-1 and occludin. Results Compared with EMAP-Ⅱ0 h group, EMAP-Ⅱ decreased the TEER value of BTB model in vitro, increased the expressing levels of p-LKB1/ LKB1 and p-AMPK/AMPK and decreased the levels of p-mTORC1/mTORC1 significantly, and the most obvious change of above indicators appeared at EMAP Ⅱ 1 h. Radicicol, compound C and IGF1 could partially block the role of EMAP-Ⅱ, caused the increase of the TEER value and the express-ing levels of tight junction associated proteins ZO-1 and occludin. Conclusion EMAP-Ⅱ might increase the permeability of BTB model in vitro, and the activation of LKB1/AMPK/mTOR signal pathway is involved in this process.