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Royal Jelly Proteins Inhibit Macrophage Proliferation: Interactions with Native- and Oxidized-Low Density Lipoprotein
The Protein Journal ( IF 3 ) Pub Date : 2021-05-18 , DOI: 10.1007/s10930-021-09998-1
Akira Sato 1, 2 , Hiroto Unuma 1 , Keiichi Ebina 1, 2
Affiliation  

Macrophage proliferation is known to correlate with macrophage accumulation in atherosclerotic plaque, and therefore its inhibition and secondary reduction of plaque inflammation may have therapeutic beneficial effects on atherosclerosis. Recently, we reported that a peptide corresponding to positions 41–51 of royalisin (which consists of 51 amino acid residues), a potent antibacterial protein contained in royal jelly (RJ), can specifically bind to oxidized LDL (Ox-LDL), a major components of atherosclerotic lesions. Here, we investigated the interaction of RJ proteins including royalisin with LDL and Ox-LDL. Measurement of LDL oxidation by the production of thiobarbituric acid reactive substances and conjugated dienes, and by electrophoretic mobility on polyacrylamide gel electrophoresis showed that RJ proteins including royalisin and the degradation products of major RJ protein (MRJP) 1 and MRJP3 can induce oxidation of LDL and Ox-LDL. Surface plasmon resonance experiments showed that these RJ proteins can exhibit much higher binding affinity to LDL than Ox-LDL (the equilibrium dissociation constant, KD = 8.35 and 49.65 μg proteins/mL for LDL and Ox-LDL, respectively). Experiments using cultured mouse J774A.1 macrophage cells proved that these RJ proteins can inhibit macrophage proliferation markedly and concentration-dependently, regardless of the absence or presence of LDL and Ox-LDL, but hardly affect lipid accumulation in macrophages. These results suggest that RJ proteins including royalisin and degradation products of MRJP1/MRJP3 may have therapeutic beneficial effects on atherosclerosis owing to the reduction of plaque inflammation. Further studies of these RJ proteins may lead to the discovery of novel anti-atherosclerotic drugs.



中文翻译:

蜂王浆蛋白抑制巨噬细胞增殖:与天然和氧化低密度脂蛋白的相互作用

已知巨噬细胞增殖与动脉粥样硬化斑块中的巨噬细胞积累相关,因此其抑制和继发减少斑块炎症可能对动脉粥样硬化具有治疗有益作用。最近,我们报道了一种对应于蜂王浆 (RJ) 中含有的强效抗菌蛋白蜂王浆 (RJ) 41-51 位的肽,可以特异性结合氧化的 LDL (Ox-LDL),动脉粥样硬化病变的主要成分。在这里,我们研究了 RJ 蛋白(包括 Royalisin)与 LDL 和 Ox-LDL 的相互作用。通过产生硫代巴比妥酸反应物质和共轭二烯来测量 LDL 氧化,聚丙烯酰胺凝胶电泳的电泳迁移率表明,包括皇家蛋白酶在内的 RJ 蛋白和主要 RJ 蛋白 (MRJP) 1 和 MRJP3 的降解产物可以诱导 LDL 和 Ox-LDL 的氧化。表面等离子体共振实验表明,这些 RJ 蛋白对 LDL 的结合亲和力比 Ox-LDL(平衡解离常数, 对于 LDL 和 Ox-LDL,K D 分别为 8.35 和 49.65 μg 蛋白质/mL)。使用培养的小鼠 J774A.1 巨噬细胞进行的实验证明,无论是否存在 LDL 和 Ox-LDL,这些 RJ 蛋白都可以显着地和浓度依赖性地抑制巨噬细胞增殖,但几乎不影响巨噬细胞中的脂质积累。这些结果表明,由于斑块炎症的减少,包括皇家蛋白酶和 MRJP1/MRJP3 降解产物的 RJ 蛋白可能对动脉粥样硬化具有治疗有益作用。对这些 RJ 蛋白的进一步研究可能会导致新的抗动脉粥样硬化药物的发现。

更新日期:2021-05-19
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