晚期糖基化终产物在多发性硬化炎性反应中的作用

The role of advanced glycation end products on inflammatory response in multiple sclerosis

多发性硬化(MS)是中枢神经系统(CNS)脱髓鞘病变。炎性反应是MS发展的重要因素,并可诱发小胶质细胞、巨噬细胞及CNS内星形胶质细胞的异常糖酵解。糖酵解过程中生成的毒性物质二羰基化合物甲基乙二醛(MGO)和乙二醛(GO)可与蛋白质中的氨基酸反应生成稳定的糖基化终末代谢产物(AGEs)。多发性硬化患者炎性反应使糖酵解增强,AGEs形成增加,而AGEs与糖基化终末产物受体(RAGE)结合进一步激活炎性反应。研究表明多发性硬化患者血液和脑组织中AGEs水平增加。因此,AGEs参与了多发性硬化的炎性反应,在MS的病理过程中具有重要的作用。本文就AGEs在MS中的作用作一综述。

Multiple sclerosis（MS） is a demyelinating disorder of the central nervous system （CNS）. The inflammatory re- sponse is an important factor in the development of MS, and can induce abnormal glycolysis of microglia, macrophages, and astrocytes in the CNS. The toxic substances dicarbonyl compounds methyl glyoxal （MGO） and glyoxal （GO） gener- ated during glycolysis react with the amino acids in the protein to form stable advanced glycation end products （AGEs）. The inflammatory response in patients with multiple sclerosis enhances glycolysis and increases the formation of AGEs, whereas the binding of AGEs to receptors for glycation endproducts（RAGE） further activates inflammatory responses. Studies have shown the levels of AGEs in blood and brain tissue in multiple sclerosis patients increase. Therefore, AGEs are involved in the inflammatory response in multiple sclerosis and play an important role in the pathogenesis of MS. The role of AGEs in MS will be reviewed.