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首页> 外文期刊>African Journal of Biotechnology >Activation of the lectin complement pathway on human renal glomerular endothelial cells triggered by high glucose and mannose-binding lectin
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Activation of the lectin complement pathway on human renal glomerular endothelial cells triggered by high glucose and mannose-binding lectin

机译：高葡萄糖和甘露糖结合凝集素触发人肾肾小球内皮细胞凝集素补体途径的激活

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This study aimed to investigate the roles of high glucose and mannose-binding lectin(MBL) on?the activation of the lectin complement pathway (LCP) on human renal glomerular endothelial cells?(HRGECs)?in vitro.?Flow cytometry analysis, immunofluorescence staining and Western blot were used to detect the cell surface deposition of MBL, C3 and the membrane attack complex (MAC), as well as the code position of MBL and C3 (MBL+C3). Electrophoretic mobility shift assay (EMSA) was used to measure the activation of nuclear factor-kappaB (NF-κB). These results show that cell surface deposition of MBL, C3 and MBL+C3 after exposure to high glucose increased in both time- and dose-dependent manner (P < 0.05). Moreover, MBL, C3 and MBL+C3 deposition stimulated by exogenous recombinant human MBL (rhuMBL) were also observed in both time- and dose-dependent manner, peaking at 4 h and then decreasing (P < 0.05). Inhibition experiments indicated that the inhibitory monoclonal antibody 3F8 against human MBL (MAb 3F8) significantly abrogated the cell surface deposition of MBL, C3 and MBL+C3, attenuated MAC staining, and inhibited NF-κB activation in HRGECs (P < 0.05). In conclusion, high glucose?and MBL?played an important role on the LCP activation?of?HRGECs, and MAb 3F8 may represent a novel potential therapeutic strategy to block LCP activation on?HRGECs.
机译：本研究旨在探讨高葡萄糖和甘露糖结合凝集素（MBL）的作用吗？凝集素补体途径（LCP）对人肾肾小球内皮细胞（HRGEC）的激活α（HRGEC）α（HRGECs）α吗？中体积计数计数分析，免疫荧光分析使用染色和蛋白质印迹来检测MBL，C3和膜攻击复合物（MAC）的细胞表面沉积，以及MBL和C3（MBL + C3）的代码位置。电泳迁移率移位测定（EMSA）用于测量核因子-κB（NF-κB）的激活。这些结果表明，在暴露于高葡萄糖后MBL，C3和MBL + C3的细胞表面沉积以时间和剂量依赖性方式增加（P <0.05）。此外，还以时间和剂量依赖性方式观察到由外源重组人MBL（RHUMBL）刺激的MBL，C3和MBL + C3沉积，在4小时达到峰值，然后减少（P <0.05）。抑制实验表明，对人MBL（MAB 3F8）的抑制单克隆抗体3F8显着消除了MBL，C3和MBL + C3，减毒MAC染色和HRGEC中的NF-κB活化的细胞表面沉积（P <0.05）。总之，高葡萄糖？和MBL？在LCP活化中发挥着重要作用？HRGECs，MAB 3F8可以代表障碍LCP激活的新潜在治疗策略。

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