CAJ | 학술논문

目的：探讨重组可溶性人CD40L（ rshCD40L）对人脐静脉内皮细胞（ HUVECs）的损伤作用及其在动脉粥样硬化中的作用。方法：应用rshCD40L刺激人脐静脉内皮细胞12 h；MTS法观察HUVECs的生存活性， ELISA法测内皮细胞E－选择素（ E－selectin）、细胞间黏附分子（ ICAM）－1、组织因子（ TF）、组织因子途径抑制物（ TF－PI）表达的变化，比色法测脂质过氧化物丙二醛（ MDA）含量及超氧化物歧化酶（ SOD）活力。结果：与正常组比较，不同浓度的rshCD40L（0．5、1、2、3 mg／L）对内皮细胞的生存活性无明显影响；0．5 mg／L rshCD40L即可增加内皮细胞E－selectin、sICAM－1、TF、TFPI的分泌，差异有统计学意义（ P＜0．01），同时增加内皮细胞MDA的含量、降低SOD活性（P＜0．05）。结论：0．5～3 mg／L rshCD40L对内皮细胞生存活性无明显影响，但已经引起内皮细胞功能障碍，增加内皮细胞炎症和外源性凝血反应，诱导内皮细胞脂质过氧化物损，使其抗氧化能力下降。
목적：탐토중조가용성인CD40L（ rshCD40L）대인제정맥내피세포（ HUVECs）적손상작용급기재동맥죽양경화중적작용。방법：응용rshCD40L자격인제정맥내피세포12 h；MTS법관찰HUVECs적생존활성， ELISA법측내피세포E－선택소（ E－selectin）、세포간점부분자（ ICAM）－1、조직인자（ TF）、조직인자도경억제물（ TF－PI）표체적변화，비색법측지질과양화물병이철（ MDA）함량급초양화물기화매（ SOD）활력。결과：여정상조비교，불동농도적rshCD40L（0．5、1、2、3 mg／L）대내피세포적생존활성무명현영향；0．5 mg／L rshCD40L즉가증가내피세포E－selectin、sICAM－1、TF、TFPI적분비，차이유통계학의의（ P＜0．01），동시증가내피세포MDA적함량、강저SOD활성（P＜0．05）。결론：0．5～3 mg／L rshCD40L대내피세포생존활성무명현영향，단이경인기내피세포공능장애，증가내피세포염증화외원성응혈반응，유도내피세포지질과양화물손，사기항양화능력하강。
[ ABSTRACT] AIM:To investigate the damage in human umbilical vein endothelial cells ( HUVECs) induced by recombinant soluble human CD40 ligand (rshCD40L).METHODS:The cultured HUVECs were treated with rshCD40L for 12 h.The survival activity of the HUVECs was observed by MTS assay.The expression of E-selectin, intercellular ad-hesion molecule (ICAM)-1, tissue factor (TF) and tissue factor pathway inhibitor (TFPI) was measured by ELISA.The activity of superoxide dismutase ( SOD) and the level of malondialdehyde ( MDA) were detected by the methods of thibabi-turic acid (TBA) .RESULTS:Compared with normal group, different concentrations of rshCD40L (0.5, 1, 2, 3 mg/L) had no obvious effect on the survival activity of the HUVECs (P>0.05).rshCD40L at concentration of 0.5 mg/L promo-ted the secretion of E-selectin, sICAM-1, TF and TFPI in the HUVECs (P<0.01).rshCD40L at concentration of 0.5 mg/L also increased MDA content and reduced the activity of SOD in the HUVECs (P<0.05).CONCLUSION:0.5~3mg/L rshCD40L has no obvious effect on endothelial cell survival, but already causes endothelial dysfunction by increas-ing endothelial inflammation and exogenous coagulation reaction, inducing lipid peroxides injury and reducing antioxidant capacity.