Selank

Selank, muaj cov amino acid sequence H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH, yog ib yam tshuaj muaj zog thiab kav ntev los tiv thaiv kev ntxhov siab.

Qhia koj txoj kev hlub

Selank, muaj cov amino acid sequence H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH, yog ib yam tshuaj muaj zog thiab kav ntev los tiv thaiv kev ntxhov siab.

Tau txais los ntawm kev tuav pov hwm thiab kev hloov kho tom ntej ntawm a tuftsin tub ntxhais tawg, txheej txheem no ho txhim kho nws lub peev xwm hla lub ntshav-hlwb barrier; tshwj xeeb hauv nruab nrab lub paj hlwb kev ua si yog ib qho ncaj qha tshwm sim ntawm kev hloov kho.

Txij li thaum pib ntawm lub xyoo pua no, ntau qhov kev sim tshuaj tau ua rau Selank; complex pharmacological zog spanning ntau modalities thiab ntau lub hom phiaj muaj peev xwm tau sau tseg.

Lub tshuab ruaj khov ntawm kev ua haujlwm yog qhov ua rau Selank tshwj xeeb muaj txiaj ntsig; Cov teebmeem rov qab tsis tshwm sim thaum txiav tawm.

Cov kab mob neurological tau txais txiaj ntsig los ntawm txoj kev tswj hwm peb zaug: neurotransmitters, neuroplasticity thiab kev tswj lub cev tiv thaiv kab mob.

Ib ntus

Thr-Lys-Pro-Arg-Pro-Gly-Pro

CAS Nr

129954-34-3

Molecular Formula

C33H57N11O9

Molecular Luj

751.887

Kev tshawb fawb ntawm Selank

1.Mechanisms of Action thiab Therapeutic Effects

Nws lub luag haujlwm tseem ceeb yog kev tswj hwm ntawm qhov sib npaug hauv cov tshuab neurotransmitter tseem ceeb hauv lub hlwb.

Modulating kis tau tus mob γ-aminobutyric acid (GABA) tshwj xeeb, nrog rau ntau yam kev tswj xyuas cov teebmeem ntawm serotonin thiab dopaminergic systems, ua rau zoo heev los tiv thaiv kev ntxhov siab thiab tshuaj tiv thaiv kev nyuaj siab.

Txhim kho hippocampal neuronal plasticity kuj tau pom; kev txawj ntse (kev kawm, nco consolidation, mloog ua piv txwv) yam tsawg kawg yog ib feem ntawm txoj cai no.

Kev tuav cia ntawm tus thawj tuftsin core tso cai rau kev ua tau zoo hauv kev tswj hwm lub cev tiv thaiv kab mob., cytokines (interferon ua ib qho ntawm cov kev kawm zoo dua) – cov nyhuv immunomodulatory lub cev tuaj yeem siv los tiv thaiv ntau yam kev ntxhov siab.

Clinical studies support the improvement of mood and enhanced psychological resilience that Selank facilitates.

2.Anti-anxiety and antidepressant effects

Unlike traditional anti-anxiety and antidepressant drugs, selank does not act directly on GABA receptors.

Hloov chaw, it works by regulating various key neurotransmitters within the brain.

Experiments have shown that selank enhances the transmission efficiency of this inhibitory neurotransmitter, GABA; inhibiting excessive neuronal activity and subsequently anxiety being the primary outcome of this process.

Further regulation of neurotransmitters – dopamine being a prime example – allows selank to significantly increase the nervous system’s stress resilience.

Mood swings and associated positive/negative feelings of pleasure are at least partially controlled; ruaj khov, long term anti-anxiety and antidepressant effects are the result.

Notable side effects (drowsiness, cognitive impairment, addiction being the most well documented) are avoided, making selank a uniquely positioned treatment for certain neurological diseases.

3.Enhancing Cognitive Function and Promoting Neuroplasticity

Selank has demonstrated efficacy in enhancing cognitive function.

Brain Derived Neurotrophic Factor (BDNF) is the focus of much of this research; upregulation of its activity is central to neuronal survival, differentiation and all forms of synaptic plasticity.

Hippocampal cells specifically show increased BDNF related activity when treated with selank.

Neural reorganization through new connections has been observed – nco consolidation, learning ability and attention/concentration all improve.

Clearer thinking, faster information processing and positive results in cognitive tests have all been recorded in patients.

4.Neuroimmune System Regulation

Tuftsin is a natural immune peptide.

Selank retains a core fragment of tuftsin, thus possessing a powerful, though subtle, immunomodulatory effect.

Neuromodulation and this neuro-immune interaction are complementary.

Chronic stress studies show Selank to be particularly well suited to psychological and physiological adaptation.

Improved or at least balanced immune responses contribute to the end result of these mechanisms.

Psychological and physical well-being are interdependent.

5.Potential for treating obsessive-compulsive disorder and agitation

Some reports indicate that selank influences the connection between the amygdala ua thiab prefrontal cortex; promoting fear extinction being one of the more directly observable effects.

Obsessive-compulsive disorder and various forms of agitation fall under this category as primary targets for treatment.

Animal experiments have shown a significant reduction of agitation-induced fur-puffing behavior, a validated measure of pure agitation.

Scientists have begun to speculate the mechanisms behind this – regulation of at least some aspect of the serotonin system being a leading theory, stress adaptation being enhanced in multiple studies.

Related research is still ongoing, but exploring these potential lines of treatment is important; treating the aforementioned diseases (psychiatric or otherwise) remains a significant and achievable goal.

COA

HPLC

MS

(1) Peb xav, C. R.; Dawb, C. M. Sedative-Hypnotic Agents Uas cuam tshuam Gamma-Aminobutyric Acid Receptors: Tsom ntsoov rau Flunitrazepam, Gamma-Hydroxybutyric Acid, Phenibut, thiab Selank. J Clin Pharmacol 2021, 61 Suppl 2, S114-S128. DOI: 10.1002/jcph.1922 Los ntawm NLM Medline.

(2) Cov pluag, A.; Kolomin, T.; Andreeva, L.; Bondarenko, E.; Myasoedov, N.; Slominsky, P.; Shadrina, M. Peptide Selank Txhim kho qhov cuam tshuam ntawm Diazepam hauv kev txo qis kev ntxhov siab nyob rau hauv Unpredictable Chronic Mild Stress Conditions nyob rau hauv nas.. Behav Neurol 2017, 2017, 5091027. DOI: 10.1155/2017/5091027 Los ntawm NLM Medline.

(3) Pin, L. G.; Nadorova, A. V.; Antipova, T. A.; Kruglov, S. V.; Kudrin, V. S.; Durnev, A. D. Selank, Peptide Analogue ntawm Tuftsin, Tiv thaiv Ethanol-Induced Memory Impairment los ntawm Regulating BDNF Cov Ntsiab Lus hauv Hippocampus thiab Prefrontal Cortex hauv nas. Bull Exp Biol Med 2019, 167 (5), 641-644. DOI: 10.1007/s10517-019-04588-9 Los ntawm NLM Medline.

(4) Pin, L. G.; Nadorova, A. V.; Seredenin, S. B. Selank Inhibits Ethanol-Induced Hyperlocomotion thiab Manifestation of Behavioral Sensitization hauv DBA/2 nas.. Bull Exp Biol Med 2016, 162 (1), 56-59. DOI: 10.1007/s10517-016-3544-6 Los ntawm NLM Medline.

(5) Nqi, N. V.; Sokolov, O.; Gabaeva, M. V.; Grivennikov, Kuv. A.; Andreeva, L. A.; Miasoedov, N. F.; Zozulia, A. A. [Semax thiab selank inhibit qhov enkephalin-degrading enzymes los ntawm tib neeg cov ntshav]]. Bioorg Khim 2001, 27 (3), 180-183. DOI: 10.1023/ib:1011373002885 Los ntawm NLM Medline.

(6) kuv tsis paub, G. G.; Teleshova, E. S.; Bochkarev, V. K.; Koschelev, V. V.; Syunyakov, T. S. P.3.036 Novel anxiolytic Selank: Cov txiaj ntsig ntawm Phase II kev sim tshuaj. European Neuropsychopharmacology 2005, 15, S159-S160. DOI: 10.1016/s0924-977x ib(05)80332-3.

(7) Slominsky, P. A.; Shadrina, M. Kuv.; Kolomin, T. A.; Stavrovskaya, A. V.; Filatova, E. V.; Andreeva, L. A.; Illarioshkin, S. N.; Myasoedov, N. F. Peptides semax thiab selank cuam tshuam rau tus cwj pwm ntawm nas nrog 6-OHDA induced PD-zoo li parkinsonism. Ntev npaum li Biol Sci 2017, 474 (1), 106-109. DOI: 10.1134/S0012496617030048 Los ntawm NLM Medline.

(8) Sollertinskaj, T. N.; Shorokhov, M. V.; Myasoedov, N. F. Cov teebmeem cerebroprotective ntawm Semax thiab Selank hauv primates ntawm ntau hom neurosis. International Journal of Psychophysiology 2008, 69 (3). DOI: 10.1016/j.ijpsycho.2008.05.356.

(9) Sollertinskaya, T. N.; Shorokhov, M. V.; Kozlovskaya, M. M.; Kozlovskii, Kuv. Kuv.; Sudakov, K. V. Compensatory thiab antiamnestic teebmeem ntawm heptapeptide Selank hauv liab. Phau ntawv Journal ntawm Evolutionary Biochemistry thiab Physiology 2008, 44 (3), 332-340. DOI: 10.1134/ib 0022093008030101.

Ib ntus:

Thr-Lys-Pro-Arg-Pro-Gly-Pro

CAS:

129954-34-3

M.W:

751.887 g/mol

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