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Repetitive hyperbaric oxygenation attenuates reactive astrogliosis and suppresses expression of inflammatory mediators in the rat model of brain injury.

Lavrnja I, Parabucki A, Brkic P, Jovanovic T, Dacic S, Savic D, Pantic I, Stojiljkovic M, Pekovic S - Mediators Inflamm. (2015)

Bottom Line: The exact mechanisms by which treatment with hyperbaric oxygen (HBOT) exerts its beneficial effects on recovery after brain injury are still unrevealed.Data obtained using real-time polymerase chain reaction, Western blot, and immunohistochemical and immunofluorescence analyses revealed that repetitive HBOT applied after the CSI attenuates reactive astrogliosis and glial scarring, and reduces expression of GFAP (glial fibrillary acidic protein), vimentin, and ICAM-1 (intercellular adhesion molecule-1) both at gene and tissue levels.Accordingly, repetitive HBOT, by prevention of glial scarring and limiting of expression of inflammatory mediators, supports formation of more permissive environment for repair and regeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurobiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, 11060 Belgrade, Serbia.

ABSTRACT
The exact mechanisms by which treatment with hyperbaric oxygen (HBOT) exerts its beneficial effects on recovery after brain injury are still unrevealed. Therefore, in this study we investigated the influence of repetitive HBOT on the reactive astrogliosis and expression of mediators of inflammation after cortical stab injury (CSI). CSI was performed on male Wistar rats, divided into control, sham, and lesioned groups with appropriate HBO. The HBOT protocol was as follows: 10 minutes of slow compression, 2.5 atmospheres absolute (ATA) for 60 minutes, and 10 minutes of slow decompression, once a day for 10 consecutive days. Data obtained using real-time polymerase chain reaction, Western blot, and immunohistochemical and immunofluorescence analyses revealed that repetitive HBOT applied after the CSI attenuates reactive astrogliosis and glial scarring, and reduces expression of GFAP (glial fibrillary acidic protein), vimentin, and ICAM-1 (intercellular adhesion molecule-1) both at gene and tissue levels. In addition, HBOT prevents expression of CD40 and its ligand CD40L on microglia, neutrophils, cortical neurons, and reactive astrocytes. Accordingly, repetitive HBOT, by prevention of glial scarring and limiting of expression of inflammatory mediators, supports formation of more permissive environment for repair and regeneration.

No MeSH data available.


Related in: MedlinePlus

Repetitive HBOT reduces gene and tissue expression of ICAM-1 after CSI. (a) Repetitive HBOT attenuated injury-induced upregulation of ICAM-1 mRNA expression in the injured cortex. Bars represent mean ± SEM of ICAM-1 mRNA (relative to GAPDH). Samples are from 4 animals per each group. Dot line represents mean of ICAM-1 mRNA level ± SEM (gray area) measured in control animals. Letters indicate significance levels (P < 0.005) between lesioned (L) and intact control groups, L versus sham control (S) group, and L compared to lesioned group subjected to the HBO protocol (LHBO). The groups not sharing a common letter are statistically different. Level of significance was analyzed using Student's t-test. (b) In the control cortex ICAM-1 localization is present on the blood vessels (asterisk). ((c) and (d)) An increased ICAM-1 immunoreactivity is seen around the lesion site after the CSI. Heavy immunostaining of blood vessels is demonstrated both in ipsilateral (asterisk (d) and (e) inset) and contralateral cortex (asterisk (e) and (e) inset). The arrow denotes dark neuron-like cells in injured (d) and contralateral cortex (e). ICAM-1-positive neutrophils, microglia ((c), (c) inset), and astrocyte-like cells ((d), arrow head) were confined to the lesion area. (f) and (g) Repetitive HBOT reduced ICAM-1 immunoreactivity, while blood vessels were faintly stained ((g) asterisk). Rectangles indicate where the high magnification images are taken from. Scale bar = 50 μm.
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fig3: Repetitive HBOT reduces gene and tissue expression of ICAM-1 after CSI. (a) Repetitive HBOT attenuated injury-induced upregulation of ICAM-1 mRNA expression in the injured cortex. Bars represent mean ± SEM of ICAM-1 mRNA (relative to GAPDH). Samples are from 4 animals per each group. Dot line represents mean of ICAM-1 mRNA level ± SEM (gray area) measured in control animals. Letters indicate significance levels (P < 0.005) between lesioned (L) and intact control groups, L versus sham control (S) group, and L compared to lesioned group subjected to the HBO protocol (LHBO). The groups not sharing a common letter are statistically different. Level of significance was analyzed using Student's t-test. (b) In the control cortex ICAM-1 localization is present on the blood vessels (asterisk). ((c) and (d)) An increased ICAM-1 immunoreactivity is seen around the lesion site after the CSI. Heavy immunostaining of blood vessels is demonstrated both in ipsilateral (asterisk (d) and (e) inset) and contralateral cortex (asterisk (e) and (e) inset). The arrow denotes dark neuron-like cells in injured (d) and contralateral cortex (e). ICAM-1-positive neutrophils, microglia ((c), (c) inset), and astrocyte-like cells ((d), arrow head) were confined to the lesion area. (f) and (g) Repetitive HBOT reduced ICAM-1 immunoreactivity, while blood vessels were faintly stained ((g) asterisk). Rectangles indicate where the high magnification images are taken from. Scale bar = 50 μm.

Mentions: As shown in Figure 3(a) CSI induced 3.34-fold (P < 0.005) increase of ICAM mRNA levels in the injured cortex, compared to the control levels. Alternatively, 10 successive treatments with HBO significantly decreased (2.85-fold, P < 0.005) ICAM mRNA expression returning it to control levels (Figure 3(a)).


Repetitive hyperbaric oxygenation attenuates reactive astrogliosis and suppresses expression of inflammatory mediators in the rat model of brain injury.

Lavrnja I, Parabucki A, Brkic P, Jovanovic T, Dacic S, Savic D, Pantic I, Stojiljkovic M, Pekovic S - Mediators Inflamm. (2015)

Repetitive HBOT reduces gene and tissue expression of ICAM-1 after CSI. (a) Repetitive HBOT attenuated injury-induced upregulation of ICAM-1 mRNA expression in the injured cortex. Bars represent mean ± SEM of ICAM-1 mRNA (relative to GAPDH). Samples are from 4 animals per each group. Dot line represents mean of ICAM-1 mRNA level ± SEM (gray area) measured in control animals. Letters indicate significance levels (P < 0.005) between lesioned (L) and intact control groups, L versus sham control (S) group, and L compared to lesioned group subjected to the HBO protocol (LHBO). The groups not sharing a common letter are statistically different. Level of significance was analyzed using Student's t-test. (b) In the control cortex ICAM-1 localization is present on the blood vessels (asterisk). ((c) and (d)) An increased ICAM-1 immunoreactivity is seen around the lesion site after the CSI. Heavy immunostaining of blood vessels is demonstrated both in ipsilateral (asterisk (d) and (e) inset) and contralateral cortex (asterisk (e) and (e) inset). The arrow denotes dark neuron-like cells in injured (d) and contralateral cortex (e). ICAM-1-positive neutrophils, microglia ((c), (c) inset), and astrocyte-like cells ((d), arrow head) were confined to the lesion area. (f) and (g) Repetitive HBOT reduced ICAM-1 immunoreactivity, while blood vessels were faintly stained ((g) asterisk). Rectangles indicate where the high magnification images are taken from. Scale bar = 50 μm.
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Related In: Results  -  Collection

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fig3: Repetitive HBOT reduces gene and tissue expression of ICAM-1 after CSI. (a) Repetitive HBOT attenuated injury-induced upregulation of ICAM-1 mRNA expression in the injured cortex. Bars represent mean ± SEM of ICAM-1 mRNA (relative to GAPDH). Samples are from 4 animals per each group. Dot line represents mean of ICAM-1 mRNA level ± SEM (gray area) measured in control animals. Letters indicate significance levels (P < 0.005) between lesioned (L) and intact control groups, L versus sham control (S) group, and L compared to lesioned group subjected to the HBO protocol (LHBO). The groups not sharing a common letter are statistically different. Level of significance was analyzed using Student's t-test. (b) In the control cortex ICAM-1 localization is present on the blood vessels (asterisk). ((c) and (d)) An increased ICAM-1 immunoreactivity is seen around the lesion site after the CSI. Heavy immunostaining of blood vessels is demonstrated both in ipsilateral (asterisk (d) and (e) inset) and contralateral cortex (asterisk (e) and (e) inset). The arrow denotes dark neuron-like cells in injured (d) and contralateral cortex (e). ICAM-1-positive neutrophils, microglia ((c), (c) inset), and astrocyte-like cells ((d), arrow head) were confined to the lesion area. (f) and (g) Repetitive HBOT reduced ICAM-1 immunoreactivity, while blood vessels were faintly stained ((g) asterisk). Rectangles indicate where the high magnification images are taken from. Scale bar = 50 μm.
Mentions: As shown in Figure 3(a) CSI induced 3.34-fold (P < 0.005) increase of ICAM mRNA levels in the injured cortex, compared to the control levels. Alternatively, 10 successive treatments with HBO significantly decreased (2.85-fold, P < 0.005) ICAM mRNA expression returning it to control levels (Figure 3(a)).

Bottom Line: The exact mechanisms by which treatment with hyperbaric oxygen (HBOT) exerts its beneficial effects on recovery after brain injury are still unrevealed.Data obtained using real-time polymerase chain reaction, Western blot, and immunohistochemical and immunofluorescence analyses revealed that repetitive HBOT applied after the CSI attenuates reactive astrogliosis and glial scarring, and reduces expression of GFAP (glial fibrillary acidic protein), vimentin, and ICAM-1 (intercellular adhesion molecule-1) both at gene and tissue levels.Accordingly, repetitive HBOT, by prevention of glial scarring and limiting of expression of inflammatory mediators, supports formation of more permissive environment for repair and regeneration.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurobiology, Institute for Biological Research "Sinisa Stankovic", University of Belgrade, 11060 Belgrade, Serbia.

ABSTRACT
The exact mechanisms by which treatment with hyperbaric oxygen (HBOT) exerts its beneficial effects on recovery after brain injury are still unrevealed. Therefore, in this study we investigated the influence of repetitive HBOT on the reactive astrogliosis and expression of mediators of inflammation after cortical stab injury (CSI). CSI was performed on male Wistar rats, divided into control, sham, and lesioned groups with appropriate HBO. The HBOT protocol was as follows: 10 minutes of slow compression, 2.5 atmospheres absolute (ATA) for 60 minutes, and 10 minutes of slow decompression, once a day for 10 consecutive days. Data obtained using real-time polymerase chain reaction, Western blot, and immunohistochemical and immunofluorescence analyses revealed that repetitive HBOT applied after the CSI attenuates reactive astrogliosis and glial scarring, and reduces expression of GFAP (glial fibrillary acidic protein), vimentin, and ICAM-1 (intercellular adhesion molecule-1) both at gene and tissue levels. In addition, HBOT prevents expression of CD40 and its ligand CD40L on microglia, neutrophils, cortical neurons, and reactive astrocytes. Accordingly, repetitive HBOT, by prevention of glial scarring and limiting of expression of inflammatory mediators, supports formation of more permissive environment for repair and regeneration.

No MeSH data available.


Related in: MedlinePlus