Hyperbaric oxygen treatment reverses radiation induced pro-fibrotic and oxidative stress responses in a rat model

Radiotherapy is effective in the treatment of tumors in the pelvic area but is associated with side effects such as cystitis and proctitis. Hyperbaric Oxygen Therapy (HBOT) has emerged as a treatment modality for radiation-induced side effects. In a rat model for radiation cystitis, we studied the e...

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Veröffentlicht in:Free radical biology & medicine 2017-02, Vol.103, p.248-255
Hauptverfasser: Oscarsson, N., Ny, L., Mölne, J., Lind, F., Ricksten, S.-E., Seeman-Lodding, H., Giglio, D.
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container_start_page 248
container_title Free radical biology & medicine
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creator Oscarsson, N.
Ny, L.
Mölne, J.
Lind, F.
Ricksten, S.-E.
Seeman-Lodding, H.
Giglio, D.
description Radiotherapy is effective in the treatment of tumors in the pelvic area but is associated with side effects such as cystitis and proctitis. Hyperbaric Oxygen Therapy (HBOT) has emerged as a treatment modality for radiation-induced side effects. In a rat model for radiation cystitis, we studied the effects of HBOT on oxidative stress and pro-fibrotic factors. Sedated Sprague-Dawley rats underwent bladder irradiation of 20Gy with and without 20 sessions of HBOT during a fortnight. Control animals were treated with and without HBOT. All four groups of animals were euthanized 28 days later. Histopathological examinations, immunohistochemistry and quantitative polymerase chain reaction (qPCR) were used to analyze changes in oxidative stress (8-OHdG), anti-oxidative responses (SOD-1, SOD2, HO-1 and NRFα) and a panel of Th1-type and Th2-type cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-13, TNF-α, TGF-β, IFN-γ) in the urinary bladder. Bladder irradiation increased the expression of 8-OHdG, SOD2, HO-1, NRFα, IL-10, TNF-α and tended to increase TGF-β. These changes were completely reversed by HBOT while HBOT in control animals had no effects on the studied markers for oxidative stress, anti-oxidative responses and Th1-type and Th2-type cytokines. Radiation induced a significant elevation of oxidative stress, antioxidants and pro-fibrotic factors in our animal model for radiation cystitis that were completely reversed and normalized by HBOT. Our findings indicate that HBOT may prevent radiation-induced changes by affecting oxidative stress and inflammatory cascades induced by radiation. Radiotherapy may cause the development of chronic inflammation and fibrosis, significantly impairing organ function. We hypothesized that bladder irradiation induces an oxidative stress reaction, thereby triggering the redox system and thus initiating an inflammatory and pro-fibrotic response. We aimed to assess whether these changes would be reversed by hyperbaric oxygen using an animal model for radiation cystitis. Our study show that hyperbaric oxygen therapy may reverse oxidative stress and pro-inflammatory factors induced by radiation. [Display omitted] •Bladder irradiation induces an oxidative stress reaction.•The oxidative stress initiates an inflammatory and pro-fibrotic response.•Hyperbaric oxygen may reverse oxidative stress induced by radiation.•Hyperbaric oxygen alone did not induce any changes in the factors studied.
doi_str_mv 10.1016/j.freeradbiomed.2016.12.036
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Hyperbaric Oxygen Therapy (HBOT) has emerged as a treatment modality for radiation-induced side effects. In a rat model for radiation cystitis, we studied the effects of HBOT on oxidative stress and pro-fibrotic factors. Sedated Sprague-Dawley rats underwent bladder irradiation of 20Gy with and without 20 sessions of HBOT during a fortnight. Control animals were treated with and without HBOT. All four groups of animals were euthanized 28 days later. Histopathological examinations, immunohistochemistry and quantitative polymerase chain reaction (qPCR) were used to analyze changes in oxidative stress (8-OHdG), anti-oxidative responses (SOD-1, SOD2, HO-1 and NRFα) and a panel of Th1-type and Th2-type cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-13, TNF-α, TGF-β, IFN-γ) in the urinary bladder. Bladder irradiation increased the expression of 8-OHdG, SOD2, HO-1, NRFα, IL-10, TNF-α and tended to increase TGF-β. These changes were completely reversed by HBOT while HBOT in control animals had no effects on the studied markers for oxidative stress, anti-oxidative responses and Th1-type and Th2-type cytokines. Radiation induced a significant elevation of oxidative stress, antioxidants and pro-fibrotic factors in our animal model for radiation cystitis that were completely reversed and normalized by HBOT. Our findings indicate that HBOT may prevent radiation-induced changes by affecting oxidative stress and inflammatory cascades induced by radiation. Radiotherapy may cause the development of chronic inflammation and fibrosis, significantly impairing organ function. We hypothesized that bladder irradiation induces an oxidative stress reaction, thereby triggering the redox system and thus initiating an inflammatory and pro-fibrotic response. We aimed to assess whether these changes would be reversed by hyperbaric oxygen using an animal model for radiation cystitis. Our study show that hyperbaric oxygen therapy may reverse oxidative stress and pro-inflammatory factors induced by radiation. 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These changes were completely reversed by HBOT while HBOT in control animals had no effects on the studied markers for oxidative stress, anti-oxidative responses and Th1-type and Th2-type cytokines. Radiation induced a significant elevation of oxidative stress, antioxidants and pro-fibrotic factors in our animal model for radiation cystitis that were completely reversed and normalized by HBOT. Our findings indicate that HBOT may prevent radiation-induced changes by affecting oxidative stress and inflammatory cascades induced by radiation. Radiotherapy may cause the development of chronic inflammation and fibrosis, significantly impairing organ function. We hypothesized that bladder irradiation induces an oxidative stress reaction, thereby triggering the redox system and thus initiating an inflammatory and pro-fibrotic response. We aimed to assess whether these changes would be reversed by hyperbaric oxygen using an animal model for radiation cystitis. Our study show that hyperbaric oxygen therapy may reverse oxidative stress and pro-inflammatory factors induced by radiation. 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source MEDLINE; Elsevier ScienceDirect Journals Complete; SWEPUB Freely available online
subjects Animals
Annan klinisk medicin
Biomedical Laboratory Science/Technology
Biomedicinsk laboratorievetenskap/teknologi
Cancer and Oncology
Cancer och onkologi
Cell and Molecular Biology
Cell- och molekylärbiologi
Cystitis
Cystitis - therapy
Cytokines - metabolism
Farmakologi och toxikologi
Female
Fibrosis
Hyperbaric oxygen
Hyperbaric Oxygenation
Medicin och hälsovetenskap
Other Clinical Medicine
Oxidative Stress
Pharmacology and Toxicology
Radiation induced injuries
Radiation Injuries, Experimental - metabolism
Radiation Injuries, Experimental - pathology
Radiation Injuries, Experimental - therapy
Rats, Sprague-Dawley
Urinary Bladder - metabolism
Urinary Bladder - pathology
Urinary Bladder - radiation effects
title Hyperbaric oxygen treatment reverses radiation induced pro-fibrotic and oxidative stress responses in a rat model
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