Ostrovskaia R U, Vakhitova Iu V, Salimgareeva M Kh, Iamidanov R S, Sadovnikov S V, Kapitsa I G, Seredenin S B
Eksp Klin Farmakol. 2010 Dec;73(12):2-5.
The influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.
已在大鼠中研究了诺肽普（N-苯基乙酰基-L-脯氨酰甘氨酸乙酯，GVS-111）——一种兼具益智药和神经保护特性的药物——对丝裂原活化蛋白激酶（MAPKs）活性以及额叶皮质、海马体和下丘脑NGF和BDNF基因及蛋白表达水平的影响。在慢性给药（28天，0.5毫克/天，腹腔注射）条件下，诺肽普降低了大鼠海马体中应激诱导激酶（SAPK/JNK 46/54和pERK1/2）的活性，并提高了下丘脑和海马体中BDNF基因的mRNA水平。下丘脑BDNF蛋白的含量也有所增加。鉴于应激诱导激酶的激活是脑组织中淀粉样蛋白生成和tau蛋白沉积的一个重要因素，以及神经营养因子缺乏在神经退行性过程发展中的作用，诺肽普给药后观察到的应激激活MAPKs活性降低和BDNF表达增加表明，这种药物对阿尔茨海默病所涉及的一些发病机制具有特定活性。
