Document Type : Original Article
Authors
1
health radiation research department, national center for radiation research and technology, atomic energy authority
2
Health Radiation Research Department, National Center for Radiation Research and Technology, Atomic energy authority
3
bHealth Radiation Research Department, National Centre for Radiation Research and Technology (NCRRT), Egyptian Atomic Energy Authority, Cairo, Egypt.
4
Health Radiation Research Department, National Center for Radiation Research and Technology,
Abstract
Radiation is capable of inducing reactive oxygen species (ROS), cytokines, chemokines, and growth factors as well as inflammatory cells. Radiation has been termed pro-inflammatory in nature. The current study aims to assess the protective effects of ivermectin against high doses of γ-irradiation by inspecting the effect on inflammatory mediators such as lung receptors toll-like receptors (TLR4), transforming growth factor beta (TGF-β), fibroblast growth factor (FGF), and nuclear factor-kappa B (NF-κβ) in adult male albino rats. Ivermectin was administered orally for 14 days at a dose of 3.7 mg/kg/day and then male albino rats were subjected to a high dose of γ-radiation (30 Gy), which was divided into 10 fractions / five times per week. In addition to increasing the activity of lactate dehydrogenase A (LDHA) in lung tissue, gamma radiation also significantly disrupted the antioxidant system, resulting in lung damage through increased levels of prostaglandin 2 (PGE2), TLR4, TGF-β, NF-κβ, and FGF. In the present work, ivermectin minimized pulmonary damage, through suppression of ROS formation and the restoration of virtually normal levels of FGF, PGE2, TGF-β, NF-κβ, and TLR4 in the lungs, as well as the activities of MAPK and LDHA. The biochemical outcomes were validated by the histological analysis. In conclusion, Ivermectin protects against γ-radiation-induced lung damage by lowering fibroblast differentiation, production of reactive oxygen species and cytokines. Ivermectin mitigates lung damage by modulating TLR4/NF-κβ /MAPK pathways.
Keywords
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