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
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 of `SEMAX®'
(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
Nerve growth factor; Brain-derived neurotrophic factor;
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 Ischemic Insult.
V.I.Skvortsova, E.L.Nasonov, E..Yu Zhuravlyeva,
I.A.Grivennikov, E.L.Arsenyeva, I.I.Sukhanov
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, Moscow .
Korsakov’s Journal of Neurology and Psychiatry
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 of SEMAX®
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 SEMAX®
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).