Dynamics of neurospecific proteins content and their formation in experimental brain injury
The aim of this study was the determination of neurospecific proteins content, mechanisms of their formation and transfer into blood in the experimental craniocerebral trauma of medium-heavy degree. Results. The accumulation of neurospecific proteins in the blood during 21 days after the trauma i...
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Zaporizhzhia State Medical and Pharmaceutical University
2016-01-01
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| Series: | Patologìâ |
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| Online Access: | http://pat.zsmu.edu.ua/article/view/71574/68180 |
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| author | S. V. Ziablitsev Ya. S. Yuzkiv O. O. Dyadyk |
| author_facet | S. V. Ziablitsev Ya. S. Yuzkiv O. O. Dyadyk |
| author_sort | S. V. Ziablitsev |
| collection | DOAJ |
| description | The aim of this study was the determination of neurospecific proteins content, mechanisms of their formation and transfer into blood in the experimental craniocerebral trauma of medium-heavy degree.
Results. The accumulation of neurospecific proteins in the blood during 21 days after the trauma is shown: S100B level increased saltatorily with two maximums – on the 1st and 7th days after the trauma, the NSE level grew gradually, the GFAP level – biphasically with maximums on the 1st and 7th days. Obviously, there was the secondary strengthening of destruction of nervous tissue and hemato-encephalic barrier permeability exactly on the 7th day. The immunohistochemical research conducted on the 7th day after the trauma showed that in the damaged neurons the S100, GFAP and NSE staining intensity disappeared or significantly diminished, which reflected sharp degenerative changes in the areas of damage. Along with this the S100 high degree staining was found around such neurons, that was characteristic for gliocytes and, in a less measure, for endotheliocytes, that can be considered as a cause of sharp increase of neurospecific proteins blood level.
Conclusions. The reason of the repeated increase of S100B blood level, in our view, could be the repeated activating of its synthesis in activated gliocytes in perifocal zones and active transport through the hemato-encephalic barrier, that activated the inflammatory damage reactions and contributed to the progression of neurodestruction on the 7th day after the trauma, reflected in the increase of GFAP blood level and further NSE accumulation. These events could signify the beginning of new pathogenesis link of the traumatic brain illness – autoimmune inflammation, that contributed to the progression of posttraumatic brain damage in the late period. |
| format | Article |
| id | doaj-art-7b7eaae21cf04eed987adf672bbb2bce |
| institution | OA Journals |
| issn | 2306-8027 2310-1237 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Zaporizhzhia State Medical and Pharmaceutical University |
| record_format | Article |
| series | Patologìâ |
| spelling | doaj-art-7b7eaae21cf04eed987adf672bbb2bce2025-08-20T02:07:04ZengZaporizhzhia State Medical and Pharmaceutical UniversityPatologìâ2306-80272310-12372016-01-0114953http://dx.doi.org/10.14739/2310-1237.2016.1.71574Dynamics of neurospecific proteins content and their formation in experimental brain injuryS. V. ZiablitsevYa. S. YuzkivO. O. DyadykThe aim of this study was the determination of neurospecific proteins content, mechanisms of their formation and transfer into blood in the experimental craniocerebral trauma of medium-heavy degree. Results. The accumulation of neurospecific proteins in the blood during 21 days after the trauma is shown: S100B level increased saltatorily with two maximums – on the 1st and 7th days after the trauma, the NSE level grew gradually, the GFAP level – biphasically with maximums on the 1st and 7th days. Obviously, there was the secondary strengthening of destruction of nervous tissue and hemato-encephalic barrier permeability exactly on the 7th day. The immunohistochemical research conducted on the 7th day after the trauma showed that in the damaged neurons the S100, GFAP and NSE staining intensity disappeared or significantly diminished, which reflected sharp degenerative changes in the areas of damage. Along with this the S100 high degree staining was found around such neurons, that was characteristic for gliocytes and, in a less measure, for endotheliocytes, that can be considered as a cause of sharp increase of neurospecific proteins blood level. Conclusions. The reason of the repeated increase of S100B blood level, in our view, could be the repeated activating of its synthesis in activated gliocytes in perifocal zones and active transport through the hemato-encephalic barrier, that activated the inflammatory damage reactions and contributed to the progression of neurodestruction on the 7th day after the trauma, reflected in the increase of GFAP blood level and further NSE accumulation. These events could signify the beginning of new pathogenesis link of the traumatic brain illness – autoimmune inflammation, that contributed to the progression of posttraumatic brain damage in the late period.http://pat.zsmu.edu.ua/article/view/71574/68180Traumatic Brain InjuriesNeurospecific Protein S100BNSE ProteinGFA Protein |
| spellingShingle | S. V. Ziablitsev Ya. S. Yuzkiv O. O. Dyadyk Dynamics of neurospecific proteins content and their formation in experimental brain injury Patologìâ Traumatic Brain Injuries Neurospecific Protein S100B NSE Protein GFA Protein |
| title | Dynamics of neurospecific proteins content and their formation in experimental brain injury |
| title_full | Dynamics of neurospecific proteins content and their formation in experimental brain injury |
| title_fullStr | Dynamics of neurospecific proteins content and their formation in experimental brain injury |
| title_full_unstemmed | Dynamics of neurospecific proteins content and their formation in experimental brain injury |
| title_short | Dynamics of neurospecific proteins content and their formation in experimental brain injury |
| title_sort | dynamics of neurospecific proteins content and their formation in experimental brain injury |
| topic | Traumatic Brain Injuries Neurospecific Protein S100B NSE Protein GFA Protein |
| url | http://pat.zsmu.edu.ua/article/view/71574/68180 |
| work_keys_str_mv | AT svziablitsev dynamicsofneurospecificproteinscontentandtheirformationinexperimentalbraininjury AT yasyuzkiv dynamicsofneurospecificproteinscontentandtheirformationinexperimentalbraininjury AT oodyadyk dynamicsofneurospecificproteinscontentandtheirformationinexperimentalbraininjury |