Zyuz'kov, G., Miroshnichenko, L., Simanina, E., Polyakova, T. (2020). PROSPECTS FOR USING MITOGEN-ACTIVATED PROTEIN KINASES ERK1/2 AND p38 OF NERVE TISSUE PROGENITORS AS PHARMACOLOGICAL TARGETS FOR THE TREATMENT OF NEURODEGENERATION CAUSED BY ALCOHOL. Bulletin of Pharmaceutical Sciences. Assiut, 43(2), 217-224. doi: 10.21608/bfsa.2020.127417
Gleb N. Zyuz'kov; Larisa A. Miroshnichenko; Elena V. Simanina; Tatyana Yu. Polyakova. "PROSPECTS FOR USING MITOGEN-ACTIVATED PROTEIN KINASES ERK1/2 AND p38 OF NERVE TISSUE PROGENITORS AS PHARMACOLOGICAL TARGETS FOR THE TREATMENT OF NEURODEGENERATION CAUSED BY ALCOHOL". Bulletin of Pharmaceutical Sciences. Assiut, 43, 2, 2020, 217-224. doi: 10.21608/bfsa.2020.127417
Zyuz'kov, G., Miroshnichenko, L., Simanina, E., Polyakova, T. (2020). 'PROSPECTS FOR USING MITOGEN-ACTIVATED PROTEIN KINASES ERK1/2 AND p38 OF NERVE TISSUE PROGENITORS AS PHARMACOLOGICAL TARGETS FOR THE TREATMENT OF NEURODEGENERATION CAUSED BY ALCOHOL', Bulletin of Pharmaceutical Sciences. Assiut, 43(2), pp. 217-224. doi: 10.21608/bfsa.2020.127417
Zyuz'kov, G., Miroshnichenko, L., Simanina, E., Polyakova, T. PROSPECTS FOR USING MITOGEN-ACTIVATED PROTEIN KINASES ERK1/2 AND p38 OF NERVE TISSUE PROGENITORS AS PHARMACOLOGICAL TARGETS FOR THE TREATMENT OF NEURODEGENERATION CAUSED BY ALCOHOL. Bulletin of Pharmaceutical Sciences. Assiut, 2020; 43(2): 217-224. doi: 10.21608/bfsa.2020.127417
PROSPECTS FOR USING MITOGEN-ACTIVATED PROTEIN KINASES ERK1/2 AND p38 OF NERVE TISSUE PROGENITORS AS PHARMACOLOGICAL TARGETS FOR THE TREATMENT OF NEURODEGENERATION CAUSED BY ALCOHOL
Goldberg Research Institute of Pharmacology and Regenerative Medicine, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia, 3 Lenin Prospect, Tomsk, 634028, Russia
Abstract
We studied the possibility of using ERK1/2 inhibitor and p38 inhibitor to modulate the functions of nerve tissue precursor cells in ethanol-induced neurodegeneration. It has been found that in chronic alcoholization of mice both these pharmacological substances are able to increase proliferative activity of neural stem cells (NSC). In addition, the blockade of ERK1/2 initiates the progression of the cell cycle of the neuronal-committed progenitors (NCP, clonogenic PSA-NCAM + cells). This reduces the differentiation intensity of NSC and clonogenic PSA-NCAM + cells under the influence of the ERK1/2 inhibitor and such in NSC under the influence of p38 inhibitor. The fundamental difference between the functions of ERK1/2 and p38 in the regulation of the NSC and NCP cell cycle in optimal living conditions and in ethanol-induced neurodegeneration does not allow to draw unambiguous conclusions about the prospect of using these protein kinases as pharmacological targets of drugs for the therapy of alcoholic encephalopathy.
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