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Protective Effects of Magnesium Sulfate on Radiation Induced Brain Injury in Rats

细胞凋亡 丙二醛 化学 医学 内分泌学 内科学 氧化应激 生物化学 有机化学
作者
Na Chen,Rui Xu,Li Wang,Meng Zhang,Feng Shi,Jin Zhou,Ting Yu
出处
期刊:Current Drug Delivery [Bentham Science Publishers]
卷期号:15 (8): 1159-1166 被引量:7
标识
DOI:10.2174/1567201815666180124112200
摘要

Objectives: The effect of magnesium sulfate on brain tissue of SD rats irradiated by 6MeV electron was investigated. Methods: SD rats were divided into three groups: control group, irradiation (IR group) and irradiation treated with magnesium sulfate (IR+M group). After being anesthetized, the whole brains of IR group and IR+M group were exposed to 6 MeV electron radiation. IR+M group was i.p. injected with 10% magnesium sulfate (400 mg/kg) one day before radiation and three days and five days after radiation. And on the 1st, 3rd, 7th and 14th day after radiation, SD rats were euthanatized to take brain tissue for the detection of calcium, redox status and cell apoptosis, as well as the expression of NF-κB and ICAM-1. Results: The results indicated that magnesium treatment may alleviate the elevation of calcium and enhance redox status through increasing the activities of superoxide dimutase (SOD) and myeloperodase (MPO), and decreasing the concentration of malondialdehyde (MDA). Tunnel and immunohistochemistry assay suggested that treatment with magnesium decreased the apoptosis rate of brain cells and the expressions of caspase-3, respectively. Decline of the expression of NF-κB and ICAM-1 protein was observed after the treatment of magnesium. Conclusion: All the results demonstrated that magnesium may elicit protective effect against radiationinduced brain injury by reducing calcium overload, improving redox and inhibiting cell apoptosis. Moreover, magnesium significantly down-regulated the protein or mRNA levels of NF-κB and ICAM- 1. The findings may provide references for the application of magnesium in clinic for brain injury induced by radiation. Keywords: Magnesium sulfate, irradiation, redox status, cell apoptosis, NF-κB/ ICAM-1, malondialdehyde (MDA).
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