Please use this identifier to cite or link to this item: https://doi.org/10.3389/fphar.2017.00352
Title: Potential protective effects of ursolic acid against gamma irradiation-induced damage are mediated through the modulation of diverse inflammatory mediators
Authors: Wang H. 
Sim M.-K. 
Loke W.K.
Chinnathambi A.
Alharbi S.A.
Tang F.R. 
Sethi G. 
Keywords: cytokine
free radical
I kappa B kinase alpha
immunoglobulin enhancer binding protein
inflammatory mediator
interleukin 1beta
interleukin 6
nitrous oxide
phosphoprotein
reactive oxygen metabolite
synaptotagmin I
tumor necrosis factor
unclassified drug
ursolic acid
animal cell
animal experiment
animal model
animal tissue
Article
cell damage
cell viability
controlled study
cytokine production
cytotoxicity
DNA binding
DNA damage
drug efficacy
enzyme linked immunosorbent assay
female
gamma irradiation
human
human cell
in vitro study
in vivo study
inflammation
lipid peroxidation
mouse
nonhuman
overall survival
protein expression
radiation dose
radiation exposure
radiation protection
Western blotting
whole body radiation
Issue Date: 2017
Publisher: Frontiers Media S.A.
Citation: Wang H., Sim M.-K., Loke W.K., Chinnathambi A., Alharbi S.A., Tang F.R., Sethi G. (2017). Potential protective effects of ursolic acid against gamma irradiation-induced damage are mediated through the modulation of diverse inflammatory mediators. Frontiers in Pharmacology 8 (JUN) : 352. ScholarBank@NUS Repository. https://doi.org/10.3389/fphar.2017.00352
Abstract: This study was aimed to evaluate the possible protective effects of ursolic acid (UA) against gamma radiation induced damage both in vitro as well as in vivo. It was observed that the exposure to gamma radiation dose- and time-dependently caused a significant decrease in the cell viability, while the treatment of UA attenuated this cytotoxicity. The production of free radicals including reactive oxygen species (ROS) and NO increased significantly post-irradiation and further induced lipid peroxidation and oxidative DNA damage in cells. These deleterious effects could also be effectively blocked by UA treatment. In addition, UA also reversed gamma irradiation induced inflammatory responses, as indicated by the decreased production of TNF-?, IL-6, and IL-1?. NF-?B signaling pathway has been reported to be a key mediator involved in gamma radiation-induced cellular damage. Our results further demonstrated that gamma radiation dose- and time-dependently enhanced NF-?B DNA binding activity, which was significantly attenuated upon UA treatment. The post-irradiation increase in the expression of both phospho-p65, and phospho-I?Ba was also blocked by UA. Moreover, the treatment of UA was found to significantly prolong overall survival in mice exposed to whole body gamma irradiation, and reduce the excessive inflammatory responses. Given its radioprotective efficacy as described here, UA as an antioxidant and NF-?B pathway blocker, may function as an important pharmacological agent in protecting against gamma irradiation-induced injury. © 2017 Wang, Sim, Loke, Chinnathambi, Alharbi, Tang and Sethi.
Source Title: Frontiers in Pharmacology
URI: https://scholarbank.nus.edu.sg/handle/10635/173879
ISSN: 16639812
DOI: 10.3389/fphar.2017.00352
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