Department of Biochemistry, School of Biology, Room 141, M.V. Lomonosov Moscow State University, Lenin's Hills, Bldg 1/12, 119992, Moscow, Russia.
Amino Acids. 2012 Jul;43(1):91-6. doi: 10.1007/s00726-011-1135-4. Epub 2011 Nov 19.
Carnosine is a known protector of neuronal cells against oxidative injury which prevents both apoptotic and necrotic cellular death. It was shown earlier that carnosine serves as an intracellular buffer of free radicals. Using the model of ligand-dependent oxidative stress in neurons, we have shown that homocysteine (HC) initiates long-term activation of extracellular signal regulated kinase, isoforms 1 and 2 (ERK 1/2) and Jun N-terminal kinase (JNK) which corresponds to exitotoxic effect resulting in cellular death. L-carnosine (β-alanyl-L-histidine) protects neurons from both excitotoxic effect of homocysteine and cellular death. Its analogs, β-alanyl-D-histidine (D-carnosine) and L-histidyl-β-alanine, restricted accumulation of free radicals and delayed activation of ERK1/2 and JNK in neuronal cells, but did not promote neuronal viability.
肌肽是一种已知的神经元细胞氧化损伤保护剂，可防止细胞凋亡和坏死。先前的研究表明，肌肽可作为自由基的细胞内缓冲剂。通过使用神经元中配体依赖性氧化应激模型，我们发现同型半胱氨酸 (HC) 可引发细胞外信号调节激酶同工型 1 和 2 (ERK1/2 和 JNK) 的长期激活，这与导致细胞死亡的细胞毒性作用相对应。L-肌肽 (β-丙氨酰-L-组氨酸) 可防止神经元受到同型半胱氨酸的兴奋性毒性和细胞死亡的影响。其类似物，β-丙氨酰-D-组氨酸 (D-肌肽) 和 L-组氨酰-β-丙氨酸，可限制自由基的积累并延迟神经元细胞中 ERK1/2 和 JNK 的激活，但不能促进神经元存活。
