Studying the Toxic Effects of Some Biologically Active Peptides on the Model of Mouse Embryonic Stem Cells


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We studied the effects of peptide drugs (HLDF-6, PGP, RPGP, and PGLP) and peptide pharmaceutical products (Semax, Selank, and thyroliberin) on proliferation and survival of mouse embryonic stem cells and their derivatives. Differentiation of mouse embryonic stem cells into neuronal precursors was evaluated. PGP and PGLP in concentrations of 10 and 0.1 μM, respectively, had little, but significant inhibitory effect on proliferative activity of cells. These peptides in concentrations of 10 and 0.1 μM, respectively, and Semax (10 and 0.1 μM) significantly increased the survival rate of mouse embryonic stem cells (serum deprivation). Moreover, study peptides had little effect on the formation of neuronal precursors from mouse embryonic stem cells. HLDF-6, Selank, and thyroliberin produced an insignificant effect on the differentiation of these cells into mature neurons. Analysis of differentiation of embryonic stem cells into GABA+ neurons showed that Selank, thyroliberin (100 μM), and NGF (100 ng/ml) decrease the ratio of these cells by 61, 58, and 87%, respectively, in comparison with the control. Our results indicate that these peptide compounds do not produce toxic effect during the embryonic and fetal period of life.

Sobre autores

A. Kobylyanskii

Institute of Molecular Genetics, Russian Academy of Sciences

Autor responsável pela correspondência
Email: testers@yandex.ru
Rússia, Moscow

Yu. Zolotarev

Institute of Molecular Genetics, Russian Academy of Sciences

Email: testers@yandex.ru
Rússia, Moscow

L. Andreeva

Institute of Molecular Genetics, Russian Academy of Sciences

Email: testers@yandex.ru
Rússia, Moscow

I. Grivennikov

Institute of Molecular Genetics, Russian Academy of Sciences

Email: testers@yandex.ru
Rússia, Moscow

N. Myasoedov

Institute of Molecular Genetics, Russian Academy of Sciences

Email: testers@yandex.ru
Rússia, Moscow


Declaração de direitos autorais © Springer Science+Business Media, LLC, 2017

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