Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study)
Objective: to study the mechanism that is responsible for impaired neuronal cell electroexcitability and viability, which is associated with modification of ADP-ribosyl cyclase in cerebral ischemic lesion, as well as the possibilities of pathogenet-ically correcting these disorders.Materials and met...
Main Authors: | , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russia
2007-12-01
|
Series: | Общая реаниматология |
Subjects: | |
Online Access: | https://www.reanimatology.com/rmt/article/view/893 |
_version_ | 1826562390826680320 |
---|---|
author | A. A. Fursov A. B. Salmina S. V. Mikhutkina L. D. Zykova N. A., Malinovskaya A. V. Morgun D. I. Laletin M. A. Fursov G. V. Yudin N. A. Shnayder S. V. Shakhmaeva |
author_facet | A. A. Fursov A. B. Salmina S. V. Mikhutkina L. D. Zykova N. A., Malinovskaya A. V. Morgun D. I. Laletin M. A. Fursov G. V. Yudin N. A. Shnayder S. V. Shakhmaeva |
author_sort | A. A. Fursov |
collection | DOAJ |
description | Objective: to study the mechanism that is responsible for impaired neuronal cell electroexcitability and viability, which is associated with modification of ADP-ribosyl cyclase in cerebral ischemic lesion, as well as the possibilities of pathogenet-ically correcting these disorders.Materials and methods. Acute cerebral ischemia was simulated in vivo on noninbred albino male rats, by ligating the right common carotid artery under general anesthesia. y-Interferon was intraperitoneally administered to the mammal in a dose of 5000 IU/kg body weight once daily for 3 days until unilateral extravasal occlusion of the common carotid artery occurred. The activity of ADP-ribosyl cyclase was evaluated by the fluorometric technique. CD38 expression in the brain cells was immunohistohemically detected. The severity of neurological symptoms was evaluated using the international NSS scale for laboratory animals. Cognitive dysfunction was recorded employing the standard test — the Morris water maze. The validity of differences was assessed by Student’s t-test and T-test, by applying STATISTICA version 6.0 (StatSoft-Russia, 1999) and BIOSTATISTICA programs.Results. Progressive neurological and cognitive deficit-induced changes occurred in the activity and expression of ADP-ribosyl cyclase/CD38 in the neuronal and glial cells in the course of brain ischemia. Neuroprotection and prevention of postischemic cognitive dysfunction were achieved by the use of y-interferon as a modifier of the brain cell expression of CD38/ADP-ribosyl cyclase. |
first_indexed | 2024-04-10T01:30:58Z |
format | Article |
id | doaj.art-e5bbaad607ed44a9a2840b4db20415b4 |
institution | Directory Open Access Journal |
issn | 1813-9779 2411-7110 |
language | English |
last_indexed | 2025-03-14T09:47:19Z |
publishDate | 2007-12-01 |
publisher | Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, Russia |
record_format | Article |
series | Общая реаниматология |
spelling | doaj.art-e5bbaad607ed44a9a2840b4db20415b42025-03-02T11:29:27ZengFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, RussiaОбщая реаниматология1813-97792411-71102007-12-013610911310.15360/1813-9779-2007-6-109-113893Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study)A. A. Fursov0A. B. Salmina1S. V. Mikhutkina2L. D. Zykova3N. A., Malinovskaya4A. V. Morgun5D. I. Laletin6M. A. Fursov7G. V. Yudin8N. A. Shnayder9S. V. Shakhmaeva10Krasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskKrasnoyarsk State Medical Academy, Federal Agency for Health Care and Social Development, KrasnoyarskA. A. Vishnevsky Central Clinical Hospital, KrasnogorskObjective: to study the mechanism that is responsible for impaired neuronal cell electroexcitability and viability, which is associated with modification of ADP-ribosyl cyclase in cerebral ischemic lesion, as well as the possibilities of pathogenet-ically correcting these disorders.Materials and methods. Acute cerebral ischemia was simulated in vivo on noninbred albino male rats, by ligating the right common carotid artery under general anesthesia. y-Interferon was intraperitoneally administered to the mammal in a dose of 5000 IU/kg body weight once daily for 3 days until unilateral extravasal occlusion of the common carotid artery occurred. The activity of ADP-ribosyl cyclase was evaluated by the fluorometric technique. CD38 expression in the brain cells was immunohistohemically detected. The severity of neurological symptoms was evaluated using the international NSS scale for laboratory animals. Cognitive dysfunction was recorded employing the standard test — the Morris water maze. The validity of differences was assessed by Student’s t-test and T-test, by applying STATISTICA version 6.0 (StatSoft-Russia, 1999) and BIOSTATISTICA programs.Results. Progressive neurological and cognitive deficit-induced changes occurred in the activity and expression of ADP-ribosyl cyclase/CD38 in the neuronal and glial cells in the course of brain ischemia. Neuroprotection and prevention of postischemic cognitive dysfunction were achieved by the use of y-interferon as a modifier of the brain cell expression of CD38/ADP-ribosyl cyclase.https://www.reanimatology.com/rmt/article/view/893ischemiabrainadp-ribosyl cyclase/cd38interferoncognitive dysfunction |
spellingShingle | A. A. Fursov A. B. Salmina S. V. Mikhutkina L. D. Zykova N. A., Malinovskaya A. V. Morgun D. I. Laletin M. A. Fursov G. V. Yudin N. A. Shnayder S. V. Shakhmaeva Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) Общая реаниматология ischemia brain adp-ribosyl cyclase/cd38 interferon cognitive dysfunction |
title | Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) |
title_full | Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) |
title_fullStr | Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) |
title_full_unstemmed | Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) |
title_short | Prevention of Postischemic Neurological Deficit by Modulating the Cerebral Cell Expression of ADP-Ribosyl Cyclase (Experimental Study) |
title_sort | prevention of postischemic neurological deficit by modulating the cerebral cell expression of adp ribosyl cyclase experimental study |
topic | ischemia brain adp-ribosyl cyclase/cd38 interferon cognitive dysfunction |
url | https://www.reanimatology.com/rmt/article/view/893 |
work_keys_str_mv | AT aafursov preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT absalmina preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT svmikhutkina preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT ldzykova preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT namalinovskaya preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT avmorgun preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT dilaletin preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT mafursov preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT gvyudin preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT nashnayder preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy AT svshakhmaeva preventionofpostischemicneurologicaldeficitbymodulatingthecerebralcellexpressionofadpribosylcyclaseexperimentalstudy |