Guevorkian Artashes G, Kanayan Alexander S, Chailian Gor G, Danielyan Kristine E, Hayrapetyan Hripsime L, Barsegyan Karine A, Khachatryan Hranush F, Galoyan Armen A, Kevorkian Guevork A
Lab. of Pathological Biochemistry, and Radioisotopic Methods, H. Buniatian Institute of Biochemistry, Natl. Acad. of Sci., Rep., of Armenia, Yerevan, RA.
Cent Nerv Syst Agents Med Chem. 2011 Sep 1;11(3):184-8. doi: 10.2174/187152411798047753.
Crush-syndrom (CS) was characterized by Bywaters E.G.L. in 1941 after London blitz. The soft tissues is followed by acute hemodynamic shock, myoglobinuria, acute renal insufficiency, and lethal endotoxicity. Data of CS pathogenesis study has shown that the largest changes in Crush occur during decompression and are accompanied by acute alteration of brain protein synthesis and strong morphological changes of brain structures. The period of decompression might be characterized by the proteolytic breakdown of the myoglobine and formation of toxic peptides. In our current work we have identified four newly formed peptides in the brain of the animals subjected to the experimental muscle tissue injury. Our investigations related with the CS experimental model have demonstrated that during the 2-hours compression protein synthesis was decreased in cytosol (32,7%) and mitochondria (49%), after 5-h compression there were registered non-significant changes in the level of protein synthesis. Intraperitoneal administration of Proline-rich peptide, ((PRP), 1 mcg/100g weight of rats), originating from proteolysis of C-terminal glycoprotein a neurophysin II along with vasopressin and oxytocin and transferring from the hypothalamus to the neurohypophysis by axonal transport, initiates activation of the protein synthesis in all studied cellular subcomponents of brain cells. The positive effect of the peptide is conditioned, most probably, by activation of the immune system and adaptation mechanisms, including mobilization of endogen-protective mechanisms of the organism.
挤压综合征（CS）于1941年由拜沃特斯（E.G.L. Bywaters）在伦敦闪电战之后进行了描述。软组织损伤后会出现急性血流动力学休克、肌红蛋白尿、急性肾功能不全和致命的内毒素血症。挤压综合征发病机制的研究数据表明，挤压过程中最大的变化发生在减压阶段，同时伴有脑蛋白合成的急性改变和脑结构的强烈形态学变化。减压期的特点可能是肌红蛋白的蛋白水解分解和有毒肽的形成。在我们目前的工作中，我们在遭受实验性肌肉组织损伤的动物脑中鉴定出了四种新形成的肽。我们与挤压综合征实验模型相关的研究表明，在2小时的压迫期间，细胞质（32.7%）和线粒体（49%）中的蛋白合成减少，在5小时的压迫后，蛋白合成水平没有显著变化。腹腔注射富含脯氨酸的肽（（PRP），1微克/100克大鼠体重），该肽源自神经垂体激素运载蛋白II C末端糖蛋白与血管加压素和催产素的蛋白水解，并通过轴突运输从下丘脑转移到神经垂体，可启动脑细胞所有研究的细胞亚成分中的蛋白合成。该肽的积极作用很可能是由免疫系统和适应机制的激活所调节的，包括机体内源保护机制的动员。
