酸敏感离子通道与过敏性紫癜患儿血管内皮损伤关系的探讨

Relationship between vascular endothelial cells of HSP patients and acid-sensing ion channels

目的探讨酸敏感离子通道(ASICs)在过敏性紫癜血管内皮细胞中的表达及在其血管内皮细胞损伤中的作用。方法免疫组化法检测HSP患儿皮肤组织中ASICs各亚型的表达和分布;以人皮肤微血管内皮细胞(HDMECs)为对象,观察不同pH条件下血管内皮细胞中ASIC1a、ASIC2a及ASIC3 mRNA的表达,同时观察ASICs阻滞剂对血管内皮细胞IL-8、NO和TM分泌及α-SMA mRNA表达的影响。结果 HSP患儿皮肤血管内皮细胞中ASIC1a及ASIC3的表达显著高于对照组,差异有统计学意义(P<0.05)。随着细胞外酸化,ASIC1a、ASIC2a及ASIC3 mRNA表达明显增加;阻断ASICs,可以显著降低血管内皮细胞中IL-8、NO和TM分泌并促进α-SMA mRNA表达。结论 ASICs可能参与了HSP患儿血管内皮细胞损伤的过程,其机制可能与诱导其进一步发生炎性反应有关。

Objective To investigate the expression of acid-sensing ion channels（ ASICs）（ ASICs） and its role in vascular endothelial cell injury of Henoch Schonlein purpura（ HSP） patients. Methods The expression of ASICs units in skin of HSP patients was measured with immunohistochemical staining. Moreover the expression of ASIC1 a,ASIC2a and ASIC3 mRNA under acidosis circumstance was examined by fluorescent quantitation PCR. In addition, the effect of ASICs inhibitors on IL-8, NO and TM level in cell culture supernatants were detected. Results High ASIC1 a,ASIC2a and ASIC3 expression in vascular endothelial cells of skin in HSP patients was found and ASIC1 a,ASIC2a and ASIC3 mRNA expression was increased with the decrement of extracellular pH. High IL-8,NO and TM level in cell culture supernatants induced by extracellular acidosis were decreased by ASICs inhibitor Amiloride and PcTX-1. And inhibiting ASICs could upregulate a-SMA mRNA expression. Conclusions ASICs could be involved in the development of HSP,its mechanism might be related to further aggravate the inflammatory response of vascular endothelial cells in HSP patients.