关键词: antioxidant apoptotic markers cerium oxide nanoparticles gamma irradiation hepatotoxicity

Mesh : Cerium / pharmacology chemistry Animals Gamma Rays / adverse effects Apoptosis / drug effects Antioxidants / pharmacology metabolism Rats Male Liver / drug effects radiation effects metabolism pathology Nanoparticles / chemistry Rats, Wistar Oxidative Stress / drug effects radiation effects Alanine Transaminase / metabolism blood Malondialdehyde / metabolism Aspartate Aminotransferases / metabolism blood Superoxide Dismutase / metabolism Proto-Oncogene Proteins c-bcl-2 / metabolism

来  源:   DOI:10.1002/cbf.4092

Abstract:
Throughout radiotherapy, radiation of the hepatic tissue leads to damage of the hepatocytes. We designed the current study to examine how cerium oxide nanoparticles (CONPs) modulate gamma irradiation-induced hepatotoxicity in rats. Animals received CONPs (15 mg/kg body weight [BW], ip) single daily dose for 14 days, and they were exposed on the seventh day to a single dose of gamma radiation (6 Gy). Results showed that irradiation increased serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities. Furthermore, it elevated oxidative stress biomarker; malondialdehyde (MDA) and inhibited the activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) in hepatic tissues homogenate. Additionally, hepatic apoptotic markers; caspase-3 (Casp-3) and Casp-9 were elevated and the B-cell lymphoma-2 (Bcl-2) gene level was decreased in rats exposed to radiation dose. We observed that CONPs can modulate these changes, where CONPs reduced liver enzyme activities, MDA, and apoptotic markers levels, in addition, it elevated antioxidant enzyme activities and Bcl-2 gene levels, as well as improved histopathological changes in the irradiated animals. So our results concluded that CONPs had the ability to act as radioprotector defense against hepatotoxicity resulted during radiotherapy.
摘要:
在整个放射治疗过程中,肝组织的辐射导致肝细胞的损伤。我们设计了当前的研究,以检查氧化铈纳米颗粒(CONP)如何调节γ辐射诱导的大鼠肝毒性。动物接受CONP(15mg/kg体重[BW],ip)每日单次剂量14天,他们在第七天暴露于单剂量的伽马射线(6Gy)。结果表明,辐射增加血清天冬氨酸氨基转移酶,丙氨酸氨基转移酶,和碱性磷酸酶活性。此外,它升高了氧化应激生物标志物;丙二醛(MDA)并抑制了肝组织匀浆中抗氧化酶(超氧化物歧化酶和谷胱甘肽过氧化物酶)的活性。此外,肝细胞凋亡标志物;在暴露于辐射剂量的大鼠中,caspase-3(Casp-3)和Casp-9升高,B细胞淋巴瘤-2(Bcl-2)基因水平降低。我们观察到CONP可以调节这些变化,CONP降低肝酶活性,MDA,和凋亡标志物水平,此外,它提高了抗氧化酶活性和Bcl-2基因水平,以及改善受照射动物的组织病理学变化。因此,我们的结果得出结论,CONP具有作为辐射防护剂防御放射治疗过程中导致的肝毒性的能力。
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