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目的研究缝隙连接蛋白(connexin,Cx)43在脂多糖(lipopolysaccharide,LPS)诱导的大鼠血管内皮细胞(vascular endothelial cell,VEC)通透性中的表达变化及其意义。方法以1、2、3、4μg/ml LPS刺激原代培养的大鼠VEC,观察作用15、30 min,1、2、3、4、5、6、7 h后VEC增殖活力和通透性的变化;2μg/ml LPS刺激VEC后,采用RT-PCR和Western blot等方法检测Cx43的表达变化;分析VEC通透性和Cx43表达之间的相关性。结果 1、2μg/ml的LPS对VEC增殖活力无明显影响,3、4μg/ml的LPS明显降低了VEC的增殖(P<0.01);2μg/ml的LPS能够较好地模拟脓毒性休克的血管高通透性(P<0.01);用此浓度的LPS刺激VEC后Cx43的mRNA和蛋白表达均逐渐降低(P<0.01);Cx43的表达与LPS引起的VEC通透性改变呈负相关关系(r=-0.877,P<0.01)。结论 Cx43可能参与了脓毒性休克后VEC通透性的调节;Cx43可能具有抑制脓毒性休克后血管内膜通透性的作用。[关键词]脓毒性休克;脂多糖;血管通透性;血管内皮细胞;连接蛋白43
Objective To study the changes of connexin (Cx) 43 in the permeability of vascular endothelial cells (VECs) induced by lipopolysaccharide (LPS) in rats and its significance. Methods Primary VECs were stimulated with LPS at 1, 2, 3, 4μg / ml for 15, 30, and 1, 2, 3, 4, 5, 6 and 7 h, respectively. VEC proliferation and permeability The changes of Cx43 expression were detected by RT-PCR and Western blot after the VEC was stimulated by 2μg / ml LPS. The correlation between VEC permeability and Cx43 expression was analyzed. Results LPS at 1 and 2 μg / ml had no significant effect on the proliferation of VEC. LPS at 3 and 3 μg / ml significantly reduced the proliferation of VEC (P <0.01). LPS at 2 μg / ml could better simulate septic shock (P <0.01). The mRNA and protein expressions of Cx43 in VEC treated with LPS at this concentration were decreased (P <0.01). The expression of Cx43 was negatively correlated with the VEC permeability induced by LPS (P < r = -0.877, P <0.01). Conclusion Cx43 may be involved in the regulation of VEC permeability after septic shock. Cx43 may have the effect of inhibiting the intimal permeability after septic shock. [Key words] septic shock; lipopolysaccharide; vascular permeability; vascular endothelial cells; connexin 43