Targeting of inflammation for radiation protection and mitigation

Yahyapour, R. and Amini, P. and Rezapoor, S. and Rezaeyan, A. and Farhood, B. and Cheki, M. and Fallah, H. and Najafi, M. (2018) Targeting of inflammation for radiation protection and mitigation. Current Molecular Pharmacology, 11 (3). pp. 203-210.

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Abstract

Background: Inflammation is the response of the immune system that guards the body against several harmful stimuli in normal conditions. However, in response to ionizing radiation that leads to a massive cell death and DNA aberrations, this phenomenon causes various side effects in normal tissues. Inflammation is involved in various side effects such as gastrointestinal toxicity, mucositis, skin reactions, nervous system damage, pneumonitis, fibrosis and so on. Discussion: Observations have proposed that inflammatory mediators are involved in the toxic effect of ionizing radiation on non-irradiated cells via a phenomenon named bystander effect. Inflammation in both irradiated and non-irradiated cells can trigger genomic instability, leading to increased risk of carcinogenesis. Targeting the inflammatory mediators has been an interesting idea for improving the therapeutic ratio throughout the reduction of normal tissue injury as well as an increase in tumor response to radiotherapy. Conclusion: So far, various targets have been proposed for the amelioration of radiation toxicity in radiotherapy. Of different targets, NF-κB, COX-2, some of NADPH Oxidase subfamilies, TGF-β, p38 and the renin-angiotensin system have shown promising results. Interestingly, inhibition of these targets can help sensitize the tumor cells to the radiation treatment with some mechanisms such as suppression of angiogenesis and tumor growth as well as induction of apoptosis. In this review, we focus on recent advances on promising studies for targeting the inflammatory mediators in radiotherapy. © 2018 Bentham Science Publishers.

Item Type: Article
Additional Information: cited By 18
Uncontrolled Keywords: 4 (4 fluorophenyl) 2 (4 methylsulfinylphenyl) 5 (4 pyridyl)imidazole; 4 4 (1,3 benzodioxol 5 yl) 5 (2 pyridinyl) 1h imidazol 2 ylbenzamide; captopril; celecoxib; curcumin; cyclooxygenase 2; diclofenac; diphenyliodonium salt; dual oxidase; dual oxidase 1; dual oxidase 2; immunoglobulin enhancer binding protein; inducible nitric oxide synthase; interleukin 1; interleukin 13; interleukin 1beta; interleukin 4; interleukin 6; interleukin 8; melatonin; prostaglandin E2; reduced nicotinamide adenine dinucleotide phosphate oxidase; reduced nicotinamide adenine dinucleotide phosphate oxidase 1; reduced nicotinamide adenine dinucleotide phosphate oxidase 2; reduced nicotinamide adenine dinucleotide phosphate oxidase 4; resveratrol; synaptophysin; transforming growth factor beta; tumor necrosis factor; unclassified drug; unindexed drug; autacoid, bystander effect; cancer radiotherapy; cell differentiation; chronic inflammation; cytokine release; disease severity; DNA damage; down regulation; drug targeting; enzyme activity; fibroblast; genomic instability; human; ionizing radiation; malignant neoplasm; nonhuman; oxidation reduction state; oxidative stress; priority journal; prostaglandin synthesis; protein expression; radiation dermatitis; radiation dose; radiation exposure; radiation injury; radiation pneumonia; radiation protection; radiation safety; radiosensitivity; renin angiotensin aldosterone system; Review; treatment response; upregulation; animal; inflammation; pathology; radiotherapy, Animals; Bystander Effect; Genomic Instability; Humans; Inflammation; Inflammation Mediators; Radiation Protection; Radiotherapy
Subjects: Medicine
Divisions: Faculty of Para medicine > Department of Management Radiology and Medical Physics
Depositing User: ART . editor
Date Deposited: 10 Apr 2019 08:05
Last Modified: 10 Apr 2019 08:05
URI: http://eprints.kaums.ac.ir/id/eprint/4098

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