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机构地区:[1]重庆医科大学附属第一医院肿瘤科,重庆400016
出 处:《细胞与分子免疫学杂志》2014年第4期375-378,共4页Chinese Journal of Cellular and Molecular Immunology
摘 要:目的探讨美洛昔康对大鼠急性放射性脑损伤的保护作用。方法 54只SD大鼠随机分为空白对照组、20 Gy照射组、治疗组(20 Gy照射后用10 mg/kg美洛昔康治疗)。用6 MeV电子束对大鼠进行20 Gy全脑单次垂直照射,分别于照射后1、3、7 d用HE染色法进行形态学观察,逆转录-聚合酶链反应(RT-PCR)分析海马组织环氧合酶2(COX-2)mRNA的表达,免疫组织化学方法观察COX-2蛋白表达。结果 HE染色结果显示,与空白对照组相比,照射组不同时间点都出现神经细胞肿胀、血管内皮细胞水肿、毛细血管周围间隙扩大,治疗组神经细胞肿胀和血管内皮细胞损伤均较照射组轻。照射后1 d,照射组和治疗组COX-2 mRNA和蛋白表达明显增强(P<0.05),与照射组相比,治疗组COX-2 mRNA、蛋白表达明显减少(P<0.05);在照射后3 d、7 d,三组间COX-2 mRNA、蛋白表达水平差异无统计学意义(P>0.05)。结论早期使用美洛昔康可减轻放疗引起的脑组织损伤,其保护作用可能与减轻血管内皮细胞损伤及COX-2表达下调有关。Objective To observe the protective effect of meloxicam against acute radiation-induced brain injury in rats. Methods Fifty-four SD rats were randomly divided into blank control group, radiation group (20 Gy) and therapy group (20 Gy radiation followed by 10 mg/kg meloxicam treatment). The whole brain of SD rats in the radiation and therapy groups were vertically irradiated by 6 MeV electron beam at a dose of 20 Gy. One, 3 and 7 days after irradiation, the morphological changes of hippocampal neurons were observed using HE staining, and the expressions of cyclooxygenase-2 (COX-2) mRNA and protein were detected by RT-PCR and immunohistochemistry, respectively. Results Compared with the blank control group, the radiation group showed that the neuron swelling and vascular endothelial cell edema as well as space enlargement around the capillaries. Both neuron swelling and vascular endothelial cell injury in the therapy group were slighter than those in the radiation group. Compared with the blank control group, the levels of COX-2 mRNA and protein in the radiation and therapy groups increased obviously one day after irradiation ( P 〈 0.0.5 ), and compared with the radiation group, the levels decreased obviously in the therapy group (P 〈 0.05 ) ; 3 and 7 days after irradiation, the levels of COX-2 mRNA and protein among the 3 groups had no statistical differences ( P 〉 0.0S). Conclusion The early use of meloxicam can reduce the brain injury induced by radiation. Its protective effect may be related to the relief of vascular endothelial cell injury and the decreased expression of COX-2.
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