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目的：：探讨甲基莲心碱对脂多糖( LPS)诱导人脐静脉内皮细胞损伤的保护机制。方法：通过预实验筛选出LPS最佳的诱导浓度；再采用最适浓度的LPS模拟人脐静脉内皮细胞炎性损伤模型,通过CCK8测定不同浓度的甲基莲心碱(0.3,1,3,5,10μmol·L-1)对损伤细胞的凋亡率的影响；Griess Reagent法用于检测一氧化氮( NO)的含量；比色法测定一氧化氮合酶( NOS)分型的活力；倒置显微镜观察细胞形态变化。结果：CCK8检测到LPS的浓度为100μg·ml-1时,细胞抑制率为54.50%,此时细胞的损伤适中,确定为诱导浓度(P<0.01)。在0.3~5.0μmol·L-1内,不同浓度的甲基莲心碱能明显提高损伤后的HUVECs的细胞活性,但在10μmol·L-1时,HUVECs细胞的增殖明显减少(P<0.05)。甲基莲心碱能显著性逆转LPS诱导的人脐血管内皮细胞中NO含量的增加和总NOS(tNOS)和iNOS的活性的升高(P<0.05)。倒置显微镜结果显示,甲基莲心碱在0.3~5.0μmol·L-1的浓度范围内,随着浓度增加,漂浮的死细胞变少,细胞形态基本良好,细胞间排列紧密。结论：甲基莲心碱能够逆转LPS诱导的人脐静脉内皮细胞的损伤,其机制可能与调节内皮细胞中NO的释放和NOS的活力有关。“,”Objective:To investigate the protective effects of neferine on lipopolysaccharide ( LPS)-induced human umbilical vein endothelial cells ( HUVECs) injury. Methods:The optimum inducing concentration of LPS was screened out through pretests and used for the model establishment of HUVECs damage. CCK8 was used to detect the influence of neferine at different concentrations on LPS-induced human umbilical vein endothelial cells ( HUVECs) injury. Nitric oxide ( NO) content was measured by the Griess Reagent method. The nitric-oxide synthase (NOS) activity was assessed by the commercially available kits. Results:The inhibitory rate of HU-VECs was 54. 50% detected by CCK8, which induced by LPS at the concentration of 100 μg·ml-1(P<0. 01). Neferine at the con-centrations of 0. 3-5. 0μmol·L-1 could increase the cell viability in a concentration-dependent manner, while it inhibited the cell pro-liferation at the concentration of 10 μmol·L-1(P<0.05). Neferine could reverse the situation, and the NO release was increased and the tNOS/iNOS activity was increased induced by LPS (P<0. 05). The results shown by the inverted microscope suggested that the floating dead cells were decreased, the cell shape was basically sound and tightly packed with the concentration increase of neferine (0. 3-5. 0μmol·L-1) in a concentration-dependent manner. Conclusion:The results show that neferine has protective effects on HU-VECs injury induced by LPS, and the mechanism may be related with the decrease of intracellular levels of NO and NOS activity.