血小板活化因子及其受体对颈髓损伤后血脊髓屏障损害的分子机制研究

目的：探讨血小板活化因子（ＰＡＦ）及其受体对颈髓损伤后血脊髓屏障损害的分子机制。方法：采用蛛网膜下腔注射ＰＡＦ及静脉注射ＰＡＦ受体拮抗剂ＢＮ５２０２１，应用地高辛标记ｃＤＮＡ探针原位杂交技术检测颈髓损伤后颈髓血管内皮细胞细胞间粘附分子－１ｍＲＮＡ（ＩＣＡＭ－１ｍＲＮＡ）和内皮细胞白细胞粘附分子－１ｍＲＮＡ（ＥＬＡＭ－１ｍＲＮＡ）表达。观察ＰＡＦ及其受体拮抗剂对颈髓损伤后血脊髓屏障、ＩＣＡＭ－１ｍＲＮＡ、ＥＬＡＭ－１ｍＲＮＡ表达的影响。结果：伤后颈髓血管内皮细胞ＩＣＡＭ－１ｍＲＮＡ、ＥＬＡＭ－１ｍＲＮＡ表达、伊文思蓝含量、水含量呈不同程度的增加；ＰＡＦ可使伤后血管内皮细胞ＩＣＡＭ－１ｍＲＮＡ、ＥＬＡＭ－１ｍＲＮＡ表达、伊文思蓝含量、水含量增加更为显著，ＰＡＦ受体拮抗剂可抑制ＩＣＡＭ－１ｍＲＮＡ、ＥＬＡＭ－１ｍＲＮＡ表达，降低颈髓组织伊文思蓝含量及水含量。结论：ＰＡＦ通过增加伤后颈髓血管内皮细胞粘附分子的表达是导致血脊髓屏障损害的重要分子基础。ＰＡＦ受体对伤后血管内皮细胞细胞粘附分子的表达具有调控作用。

Molecular Mechanism Studies of Platelet Activating Factor and Its Receptor on Damage of Blood Spinal Cord Barrier Following Cervical Cord Injury

Objective: To investigate the molecular mechanism of platelet activating factor (PAF) and its receptor on blood spinal cord barrier damage after cervical cord injury. Methods: PAF and PAF receptor antagonist BN52021 were administered through arachnoid space and intravenous injection respectively. The expression of intercellar adhesion molecule-1mRNA (ICAM-1mRNA) and endothelial cell leukocyte adhesion molecule-1mRNA(ELAM-1mRNA) in cervical cord vascular endothelial cells were measured by digoxigein labelled cDNA probe in situ hybridization technique after trauma. The effects of PAF and its receptor antagonist on blood spinal cord barrier, ICAM-1mRNA, ELAM-1mRNA after cervical cord injury were observed. Results: The expression of ICAM-1mRNA, ELAM-1mRNA in cervical cord vascular endothelial cells, Even blue levels and water contert in cervical tissue increased in varying degrees after trauma, the expression of ICAM-1mRNA, ELAM-1mRNA in cervial cord vascular endothelial cells, Even blue levels and water content in cervical tissue were remarkbly elevated by PAF through arachnoid space injection. PAF receptor antagonist BN52021 could inhibit the expression of ICAM-1mRNA and ELAM-1mRNA in cervical cord vascular endothelial cells, which significantly decreased Even content and water content in cervical cord tissues after trauma. Conclusions: The increase of expression of cell adhesion molecules by PAF in cervical cord vascular endothelial cells was an important molecular basis of blood spinal cord barrier damage after trauma. PAF receptor has the potential to control and adjust the expression of cell adhesion molecules in cervical cord vascular endothelial cells following trauma.