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目的观察活化蛋白C(APC)是否能够通过核因子-κB(NF-κB)途径抑制TNF-α介导的炎症反应。方法分离培养正常组、TNF-ɑ组、TNF-ɑ+rhAPC组的人脐静脉内皮细胞细胞(HUVECs)。用ELISA法,检测细胞上清液中的细胞内粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)及选择素浓度。用逆转录聚合酶链反应、Western bloting技术检测HUVECs NF-κBmRNA、NF-κB蛋白的表达。结果细胞上清液中ICAM-1、VCAM-1及E选择素浓度,TNF-ɑ组较正常组显著升高(均P<0.05);而TNF-ɑ+rhAPC组较TNF-ɑ组显著降低(均P<0.05)。HUVECs NF-κB mRNA、蛋白表达水平,TNF-ɑ组较正常组均显著升高(均P<0.05);而TNF-ɑ+rhAPC组较TNF-ɑ组均显著降低(均P<0.05)。结论 APC通过抑制黏附分子的产生来调节TNF-α介导的炎症反应,其可能是通过NF-κB途径来实现。
Objective To investigate whether activated protein C (APC) inhibits TNF-α-mediated inflammation through the nuclear factor-κB (NF-κB) pathway. Methods Human umbilical vein endothelial cells (HUVECs) were isolated and cultured in normal group, TNF-ɑ group and TNF-ɑ + rhAPC group. Cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and selectin concentrations in the cell supernatant were detected by ELISA. Reverse transcription polymerase chain reaction and Western blotting were used to detect the expression of NF-κBmRNA and NF-κB in HUVECs. Results The levels of ICAM-1, VCAM-1 and E-selectin in the supernatant were significantly higher in the TNF-ɑ group than those in the normal group (all P <0.05), while those in the TNF-ɑ + rhAPC group were significantly lower than those in the TNF- (All P <0.05). The expression of NF-κB mRNA and protein in HUVECs was significantly higher than that in the normal group (all P <0.05), while TNF-ɑ + rhAPC group was significantly lower than that in the TNF-ɑ group (all P <0.05). Conclusion APC can regulate the TNF-α-mediated inflammatory response by inhibiting the production of adhesion molecules, which may be achieved through the NF-κB pathway.