PURPOSE: Radiotherapy is effective in the treatment of @entity5 in the pelvic area but is associated with side effects such as @entity2335 and @entity4272 . Hyperbaric @entity26 Therapy (HBOT) has emerged as a treatment modality for radiation-induced side effects. In a @entity35 model for @entity2335 , we studied the effects of HBOT on oxidative stress and pro-fibrotic factors. MATERIALS AND METHODS: Sedated @entity35 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 ( @entity20821 ), anti-oxidative responses ( @entity24544 , @entity26486 , @entity22456 ) and a panel of Th1-type and Th2-type cytokines ( @entity3426 , @entity12718 , @entity22538 , @entity568 , @entity13358 , @entity10957 , @entity1505 , @entity1810 , IFN-y) in the urinary bladder. RESULTS: Bladder irradiation increased the expression of @entity20821 , @entity26486 , HO-1, NRFa, @entity13358 , @entity1505 and tended to increase @entity1810 . 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. CONCLUSIONS: Radiation induced a significant elevation of oxidative stress, antioxidants and pro-fibrotic factors in our animal model for @entity2335 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. SUMMARY: Radiotherapy may cause the development of @entity32 and @entity82 , 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 @entity26 using an animal model for @entity2335 . Our study show that hyperbaric @entity26 therapy may reverse oxidative stress and pro-inflammatory factors induced by radiation.

Hyperbaric XXXX treatment reverses radiation induced pro-fibrotic and oxidative stress responses in a @entity35 model.

@entity20821 :: ('MESH:C067134', 'Chemical') :: ['8-OHdG'] @entity26486 :: ('24787(Tax:10116)', 'Gene') :: ['SOD2'] @entity32 :: ('MESH:D007249', 'Disease') :: ['chronic inflammation'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumors'] @entity4272 :: ('MESH:D011349', 'Disease') :: ['proctitis'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen', 'Oxygen'] @entity12718 :: ('287287(Tax:10116)', 'Gene') :: ['IL-4'] @entity568 :: ('24498(Tax:10116)', 'Gene') :: ['IL-6'] @entity22456 :: ('24451(Tax:10116)', 'Gene') :: ['HO-1 and NRFa'] @entity13358 :: ('25325(Tax:10116)', 'Gene') :: ['IL-10'] @entity1505 :: ('24835(Tax:10116)', 'Gene') :: ['TNF-a'] @entity24544 :: ('24786(Tax:10116)', 'Gene') :: ['SOD-1'] @entity3426 :: ('24494(Tax:10116)', 'Gene') :: ['IL-1b'] @entity1810 :: ('59086(Tax:10116)', 'Gene') :: ['TGF-b'] @entity22538 :: ('24497(Tax:10116)', 'Gene') :: ['IL-5'] @entity35 :: ('10116', 'Species') :: ['Sprague-Dawley rats', 'rat'] @entity2335 :: ('MESH:D003556', 'Disease') :: ['cystitis', 'radiation cystitis'] @entity10957 :: ('116553(Tax:10116)', 'Gene') :: ['IL-13']
@entity26 :: (MESH:D010100,Chemical) :: ['oxygen']
