关于 LOX-1的背景资料：低密度脂蛋白(oxidized low density lipop rotein, ox2LDL)的特异性受体———血凝素样ox2LDL 受体1 ( lectin2likeoxi2 dized low density lipop rotein recep tor21,LOX21)可通过损伤血管内皮,促进炎症反应,加速细胞凋亡和泡沫细胞形成等机制促进动脉粥样硬化的发展,进而导致冠心病的发生、发展。炎症因子、一氧化氮缺乏等因素可促进LOX-1表达，一些相关药物通过抑制LOX-1的表达在动脉粥样硬化中起作用，为临床抗动脉粥样硬化治疗提供新的途径。因此这个受体是研究动脉硬化的关键分子。

研究摘要：氢气是一种良好的生物抗氧化物质，氧化型低密度脂蛋白通过结合细胞表面受体LOX-1在动脉硬化的发生过程中具有重要作用。多种刺激因子如TNF-a可以促进 LOX-1的表达。本研究各种刺激因子诱导内皮细胞的LOX-1表达上调是否可以被氢气阻断。结果发发现，氢气对TNF-a等各种刺激因子引起的内皮细胞LOX-1基因表达和蛋白水平上调均具有显著的抑制作用，NF-kB的抑制剂 NAC对TNF-a引起的内皮细胞LOX-1基因表达和蛋白水平上调同样具有抑制作用。氢气对TNF-a引起的内皮细胞NF-k B激活和IkB-a磷酸化具有抑制作用。氢气对apo E基因敲除动脉硬化小鼠的LOX-1表达和NF-kB活性也具有抑制作用。因此氢气可能通过抑制NF-k B对减少炎症因子诱导的LOX-1表达，发挥对动脉硬化的治疗作用。

该研究更深入地研究了氢气治疗疾病的分子机制，并采用基因敲除动脉验证了细胞水平上的结果，丰富了人们对氢气治疗疾病的分子机制的认识，确定了氢气抗炎症的分子途径。是一篇非常重要的研究报道。全文：

H2 inhibits TNF-a-induced lectin-like oxidized LDL receptor-1 expression by inhibiting nuclear factor kB activation in endothelial cells

Guohua Song • Hua Tian • Jia Liu • Hongle Zhang • Xuejun Sun • Shucun Qin

Abstract H2 is a therapeutic antioxidant that can reduce oxidative stress. Oxidized low-density lipoprotein, which plays roles in atherosclerosis, may promote endothelial dysfunction by binding the cellsurface receptor LOX-1. LOX-1 expression can be upregulated by various stimuli, including TNF-a. Thus, we aimed to examine whether the upregulation of LOX-1 by different stimuli could be blocked by H2 in endothelial cells. H2 significantly abolished the upregulation of LOX-1 by different stimuli, including TNF-a, at the protein and mRNA levels. The TNF-ainduced upregulation of LOX-1 was also attenuated by the NF-kB inhibitor N-acetyl-L-cysteine. H2 inhibited the TNF-a-induced activation of NF-kB and the phosphorylation of IkB-a. Furthermore, H2 inhibited the expression of LOX-1 and the activation of NF-kB in apolipoprotein E knockout mice, an animal model of atherosclerosis. Thus, H2 probably inhibits cytokine-induced LOX-1 gene expression by suppressing NF-kB activation.