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Radioprotective effect of diethylcarbamazine on radiation-induced acute lung injury and oxidative stress in mice

机译:二乙基氨基吡啶对小鼠辐射诱导急性肺损伤和氧化应激的辐射防护作用

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摘要

The present study was designed to evaluate the radioprotective effect of diethylcarbamazine (DEC) against oxidative stress and acute lung injury induced by total body radiation (TBI) in mice. For study the optimum dose for radiation protection of DEC, mice were administrated with three dose of DEC (10, 50 and 100 mg/kg), once daily for eight consecutive days. Animals were exposed whole body to 5 Gy X-radiation on the 9 day. The radioprotective potential of DEC in lung tissues was assessed using oxidative stress examinations at 24 h after TBI and histopathological assay also was analyzed one week after TBI. Results from biochemical analyses demonstrated increased malonyldialdehyde (MDA), nitric oxide (NO) and protein carbonyl (PC) levels of lung tissues in only irradiated group. Histopathologic findings also showed an increase in the number of inflammatory cells and the acute lung injury in this group. DEC pretreatment significantly mitigated the oxidative stress biomarkers as well as histological damages in irradiated mice. The favorable radioprotective effect against lungs injury was observed at a dose of 10 mg/kg of DEC in mice as compared with two other doses (50 and 100 mg/kg). The data of this study showed that DEC at a dose of 10 mg/kg with having antioxidant and anti-inflammatory properties can be used as a therapeutic candidate for protecting the lung from radiation-induced damage.
机译:本研究旨在评估二乙基氨基吡吡啶(DEC)对小鼠总体辐射(TBI)诱导的氧化应激和急性肺损伤的辐射防护作用。为了研究DEC的辐射保护的最佳剂量,小鼠用三剂DEC(10,50和100mg / kg),每天持续持续3天。将动物暴露于9天的5 Gy X-辐射。在TBI和组织病理学测定后24小时,在TBI后一周在24小时下,在TBI后一周分析肺组织中DEC的放射性保护潜力。生物化学分析的结果证明仅在辐照基团中显示了肺组织的含锰醛(MDA),一氧化氮(NO)和蛋白质羰基(PC)水平。组织病理学发现还显示出该组炎性细胞数量和急性肺损伤的增加。 DEC预处理显着降低了氧化应激生物标志物以及照射小鼠的组织学损伤。与另外两剂(50和100mg / kg)相比,在小鼠中,在小鼠中的10mg / kg DEC的剂量下观察到对肺损伤的有利辐射保护作用。该研究的数据表明,具有抗氧化剂和抗炎特性的10mg / kg剂量的DEC可以用作保护肺部免受辐射诱导的损伤的治疗候选者。

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