摘要
目的 探索信号分子蛋白激酶C(protein kinase C,PKC)在内皮-单核细胞激活多肽Ⅱ(endothelial monocyte activating polypeptide-Ⅱ,EMAP-Ⅱ)增强血肿瘤屏障(blood-tumor barrier,BTB)通透性中的作用。方法 荷瘤大鼠被随机分成3组C每组8只):对照组、EMAP-Ⅱ组、H7+EMAP-Ⅱ组。采用伊文思蓝(Evans blue,EB)渗透性实验评估实验各组BTB通透性的变化;Western Blot法、免疫组织化学法及免疫荧光法检测脑微血管内皮细胞上紧密连接相关蛋白occludin表达水平的变化。结果 与对照组和H7+EMAP-Ⅱ组相比较,EMAP-Ⅱ组BTB通透性显著增高,紧密连接相关蛋白occludin的表达水平显著降低,EMAP-Ⅱ的作用受到PKC抑制剂H7预处理的显著抑制。结论 信号分子PKC在EMAP-Ⅱ增强BTB通透性中发挥着重要的作用。
Objective To detect the role and mechanism of protein kinase C(PKC) in the endothelial monocyte-activating polypeptide-Ⅱ(EMAP-Ⅱ) -induced increase in blood-tumorbarrier(BTB) permeability. Methods Tumor-bearing rats were randomly divided into 3 groups(n = 8): control, EMAP-Ⅱ, and HT+EMAP-Ⅱ groups. Evans blue(EB) assay was used to evaluate the changes of BTB permeability. The expression of fight junction-related protein occludin in brain microvascular endothelial cells was measured by western blot, immunohistoehemistry and immunofluorescent assays. Results EMAP-Ⅱ significantly increased permeability of the BTB and decreased the expression level of occludin in brain microvascular endothelial cells, pretreatment with H7(the inhibitor of PKC) blocked EMAP-Ⅱ-indueed increase of BTB permeability and inhibited EMAP-Ⅱ-induced downregulation of occludin expression level significantly. Conclusions PKC signaling molecule plays an important role in EMAP-Ⅱ-induced increase in the BTB permeability.
出处
《解剖科学进展》
CAS
2012年第5期412-415,共4页
Progress of Anatomical Sciences
基金
国家自然科学基金资助项目(No.81172197
81171131
30973079)
高等学校博士学科点专项科研基金(No.20092104110015
20102104110009)
沈阳市科学技术计划项目计划(No.F10-205-1-37
F10-205-1-22)