Clinical documentation in published form has started
to enter the International Medical community as interest in this
novel peptide grows. It is unfortunate that according to legal provisions
of the Russian Federation, the records of the Federal Commission
for Drug Registration and Application on preliminary clinical trials
are prohibited from publication for a period of 10 years.
induction of neurotrophin mRNAs in rat glial cell cultures by SEMAX®,
an adrenocorticotropic hormone analog.
I. Shadrina, Oleg V. Dolotov, Igor A. Grivennikov, Petr
A. Slominsky*, Ludmila A. Andreeva, Ludmila S. Inozemtseva, Svetlana
A. Limborska, Nikolay F. Myasoedov
Institute of Molecular Genetics, Russian Academy of Sciences, Kurchatov
square 2, 123182 Moscow, Russia.
Neuroscience Letters 308 (2001) 115±118
Received 16 February 2001; received in revised form 1 June 2001;
accepted 7 June 2001
The proliferation, differentiation and survival of neuronal and
glial cells are affected by a number of neurotrophic factors, such
as nerve growth factor (NGF), brain-derived neurotrophic factor
(BDNF) and others. In a previous study, we observed the effects
(Met-Glu-His-Phe-Pro-Gly-Pro), the physiologically active analogue
of adrenocorticotropic hormone(4-10), on neuronal cell survival
in vitro. We hypothesized that these effects may be mediated by
the regulation of expression of some neurotrophic factors. To test
this hypothesis we analyzed NGF and BDNF gene expression in glial
cells obtained from the basal forebrain of newborn rats, following
in vitro treatment with `SEMAX®'.
We observed changes in mRNA levels for both the NGF and BDNF genes.
The greatest increase in expression was found after 30 min of `SEMAX®'
administration. At this time, BDNF mRNA level was increased eight-fold
in comparison with control, and NGF mRNA level was increased five-fold.
2001 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Gene expression; Glial cells; Adrenocorticotropic hormone(4±10);
Nerve growth factor; Brain-derived neurotrophic factor; Neurotrophic
synthetic analogue of ACTH 4-10 (SEMAX®)
but not glycine prevents the enhanced nitric oxide generation in
cerebral cortex of rats with incomplete global ischemia.
c Valentina G. Bashkatova , Vladimir B. Koshelev
, Olga E. Fadyukova ,
a b Alexandr A. Alexeev , Anatolii F. Vanin , Kirill S. Rayevsky
, Igor P. Ashmarin ,
b ,* David M. Armstrong
a Institute of Pharmacology , Russian Academy of Medical Sciences
, 8 Baltiyskaya Street , 125315 Moscow , Russia. b Lankenau Institute
for Medical Research , Thomas Jefferson University ,Wynnewood ,
PA 19096,USA. c Department of Physiology , Lomonosov Moscow State
University , Moscow , Russia Accepted 12 December 2000.
Brain Research 894 (2001) 145–149
This work investigates whether nitric oxide production and lipid
peroxidation contribute to the pathophysiology of ischemia and whether
glycine and a novel Russian compound, Semax are neuroprotective
via a mechanism involving the regulation nitric oxide (NO) and lipid
peroxidation. In brief, nitric oxide and indices of lipid peroxidation
were elevated following global ischemia. While glycine proved ineffective
in reducing NO levels or ameliorating the neurological deficits
following global ischemia, SEMAX®
proved to be highly effective in abating the rise in nitric oxide
and restoring neurologic functioning. Ó 2001 Elsevier Science
B.V. All rights reserved.
Theme : Disorders of the nervous system
Topic : Ischemia
Keywords : Nitric oxide (NO); Electron paramagnetic resonance spectroscopy;
Lipid peroxidation; SEMAX®;
of Neuroprotective Effects of Semax® in the Acute Period of
V.I.Skvortsova, E.L.Nasonov, E..Yu Zhuravlyeva, I.A.Grivennikov,
The Chairs of Neurology and Neurosurgery Nos. 1 and 2 of the Russian
State Medical University, Moscow Medical Academy "I. M. Secenova",
Institute of Molecular Genetics of the Russian Academy of Sciences,
Korsakov’s Journal of Neurology and Psychiatry 5.
is the first domestic nootropic drug from the group of neuropeptides.
Experimental assays showed that in doses of 100-150 ug/kg body weight
it had angioprotective, antihypoxic and neurotrophic effects. Complex
neuro-physiological investigations demonstrated its high effectiveness
in acute ischemic insult. This paper presents a clinical trial of
the immunobiochemical mechanisms of the neuroprotective effects
in the acute period of an ischemic stroke. A retrospective comparison
of clinical immunobiochemical analyses made it possible to obtain
unbiased data, at the molecular level, on activating effects of
on the anti-inflammatory chain of post-ischemic reactions in the
brain, changes in the neuromediatory balance towards the prevalence
of anti-inflammatory agents (interleukin-10, Transforming Growth
Factor-ß1) over the factors maintaining the inflammatory process
(interleukin-8, C-reactive protein).