Experimental assessment of the KK1 peptide effectiveness for prevention of the CNS delayed impairments after acute intoxication with carbon monoxide

Pavel Gennadievich Tolkach; Vadim Alexandrovich Basharin; Alexandre Nikolayevich Grebenyuk; Alexandre Alexandrovich Kolobov

doi:10.17816/RCF13329-34

Reviews on Clinical Pharmacology and Drug Therapy ›› 2015, Vol. 13 ›› Issue (3) : 29 -34. DOI: 10.17816/RCF13329-34

Articles

research-article

Experimental assessment of the KK1 peptide effectiveness for prevention of the CNS delayed impairments after acute intoxication with carbon monoxide

Author information +

History +

PDF

Abstract

Intoxication with the carbon monoxide leads to the development the early and delayed neuropsychological impairments. Oxygen therapy is used usually as an antidote for the treatment of acute carbon monoxide poisoning. The synthetic analogues of endogenous peptides were shown to prevent the neuropsychological impairments. One of them is KK1, a tetrapeptide acetyl-(D-Lys)-Lys-Arg-Arg-amide, assessed as a structural analogue of corticotropine. The efficiency of the synthetic tetrapeptide KK1 for the prevention of the CNS delayed impairments after acute carbon monoxide poisoning has been evaluated in this study.

Keywords

carbon monoxide / neurotoxicity / cognitive impairments / oxygen / synthetic tetrapeptide KK1

Cite this article

Download citation ▾

Pavel Gennadievich Tolkach, Vadim Alexandrovich Basharin, Alexandre Nikolayevich Grebenyuk, Alexandre Alexandrovich Kolobov. Experimental assessment of the KK1 peptide effectiveness for prevention of the CNS delayed impairments after acute intoxication with carbon monoxide. Reviews on Clinical Pharmacology and Drug Therapy, 2015, 13(3): 29-34 DOI:10.17816/RCF13329-34

登录浏览全文

4963

注册一个新账户忘记密码

References

Publishing order | Descend order by publishing year | Descend order by cited within

[1]	Буреш Я., Бурешова О., Хьюстон Д. П. Методики и основные эксперименты по изучению мозга и поведения: пер. с англ. Е. Н. Живописцевой / Под ред. А. С. Батуева. М.: Высшая школа, 1991. - 400 с.

[2]	Дейко Р. Д., Штрыголь С. Ю., Колобов А. А., Симбирцев А. С. Церебропротективные свойства оригинальных пептидов, гомологичных первичной последовательности участка АКТГ15-18 (экспериментальное исследование). Цитокины и воспаление. 2015; 14 (1): 27-30.

[3]	Методические указания о количественном определении карбоксигемоглобина и карбоксимиоглобина. М.: МЗ СССР, 1974. - 16 с.

[4]	Прозоровский В. Б. Статистическая обработка результатов фармакологических исследований. Психофармакол. и биол. наркол. 2007; 7 (3-4): 2090-2120.

[5]	Софронов Г. А., Черный В. С., Александров М. В. Качество жизни лиц, перенесших острые отравления продуктами горения. Вестн. Рос. воен.-мед. акад. 2012; 2 (38): 6-10.

[6]	Тетрапептид и средство, обладающее церебропротекторной и антиамнестической активностью (варианты). Патент РФ № 2537560 от 27.10.2014. - БИ № 30. - 13 с.

[7]	Borbely E., Scheich B., Helyes Z. Neuropeptides in learning and memory. Neuropeptides. 2013; 47: 439-50.

[8]	Braubach M., Algoet A., Beaton M. [et al] Mortality associated with exposure to carbon monoxide in WHO European member states. Indoor Air. 2013; 23: 115-25.

[9]	Heung M. L., Lance M. H., George H. J. Differential inhibition of mitochondrial respiratory complexes by inhalation of combustion smoke and carbon monoxide, in vivo, in the rat brain. Inhal. Toxicol. 2010; 22 (9): 770-7.

[10]	Juric D. M., Finderle Z., Suput D. et al. The effectiveness of oxygen therapy in carbon monoxide poisoning is pressure- and time-dependent: A study on cultured astrocytes. Toxicol. Lett. 2015; 233 (1): 16-23.

[11]	Lindell K., Weaver L. K. Clinical practice. Carbon monoxide poisoning. N. Engl. J. Med. 2009; 360 (12): 1217-25.

[12]	Mariluz H. V., Castoldy A. F., Cocini T. In vivo exposure to carbon monoxide causes delayed impairment of activation of soluble guanylatecyclase by nitric oxide in rat brain cortex and cerebellum. J. Neurochem. 2004; 89 (5): 1157-65.

[13]	Morellini F. Spatial memory tasks in rodents: what do they model? Cell Tissue Res. 2013; 34: 273-86.

[14]	Ochi S., Abe M., Li C. et al. The nicotinic cholinergic system is affected in rats with delayed carbon monoxide encephalopathy. Neurosci Lett. 2014; 569: 33-7.

[15]	Piantadosi C. A., Zhang J., Levin E. D. et al. Apoptosis and delayed neuronal damage after carbon monoxide poisoning in the rat. Experimental Neurology. 1997; 147 (1): 103-14.

[16]	Picciotto, M. R., Zoli M., Lena C. et al. Abnormal avoidance learning in mice lacking functional high-affinity nicotine receptor in the brain. Nature. 1995; 374 (6517): 65-7.

[17]	Roozendaal B., Schelling G., McGaugh J. L. Corticotropin-realising factor in the basolateral amygdala enhances memory consolidation via an interaction with the β-adrenoceptor-cAMP pathway: dependence on glucocorticoid receptor activation. J. Neurosci. 2008; 28 ( 26): 6642-51.

[18]	Sungho O. Choi S. Acute carbon monoxide poisoning and delayed neurological sequelae: a potential neuroprotection bundle therapy. Neural Regen. Res. 2015; 10 (1): 36-8.