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作 者:董国福 王长振 赵曦 周红梅 赵雪龙 DONG Guo-fu;WANG Chang-zhen;ZHAO Xi;ZHOU Hong-mei;ZHAO Xue-long(Institute of Radiation Medicine,Academy of Military Medical Sciences,Beijing 100850,China)
机构地区:[1]军事科学院军事医学研究院辐射医学研究所,北京100850
出 处:《微波学报》2021年第1期93-96,共4页Journal of Microwaves
基 金:北京市自然科学基金(5194029)。
摘 要:探讨了海藻硫酸多糖(SP)对高功率微波(HPM)致小鼠精母细胞系GC-2细胞的损伤防治作用及其机制,为新型抗电磁辐射药物开发提供基础。将GC-2细胞分为药物组、药物对照组、辐射组和正常对照组,采用平均功率密度为30 mW/cm2的S波段HPM辐照15 min,药物组和药物对照组于照射前24 h加入SP(终浓度25μg/ml)。辐照后立即检测细胞的活性氧(ROS)、凋亡相关蛋白Caspase3、p53、Bax和Bcl-2及氧化应激信号通路MAPK中蛋白p-38MAPK和p-JNK1/2等指标的活化,并于1 h、3 h、6 h、12 h、24 h检测细胞活力。与正常组相比,辐照后6 h辐射组细胞活力显著降低,细胞即刻的ROS、Caspase3、p53、Bax、p-38MAPK和p-JNK1/2表达显著升高,Bcl-2显著降低;与辐射组相比,药物组和药物对照组细胞即刻的ROS、Caspase3、p53、Bax、p-38MAPK以及p-JNK1/2的表达显著降低,Bcl-2显著升高。结果表明,30 mW/cm2 S-HPM辐射可引起GC-2细胞产生氧化应激损伤,预防性给予SP可通过抗氧化机制对HPM辐射损伤起保护作用。This work is to investigate the protective effect and mechanism of sulfated polysaccharide(SP)on HPM-induced GC-2 cell injury.The mouse spermatogenic GC-2 cells were divided into drug group,drug control group,radiation group and control group.All cells were exposed S-band HPM with an average power density of 30 mW/cm2 for 15 min.The drug group and the drug control group were added to the SP concentration of 25μg/ml at 24 h before microwave irradiation.After exposure,the ROS content,expression of apoptosis-related proteins Caspase3,p53,Bax and Bcl-2,and p-38MAPK and p-JNK1/2 in MAPK signaling pathway of cellular oxidative stress were detected immediately.Cell viability was measured at 1 h,3 h,6 h,12 h,and 24 h after exposure.Compared with the normal group,the proliferation activity of the irradiated group at 6h was significantly decreased,and the immediate ROS content of the cells and the expression of Caspase 3,p53,Bax,p-38MAPK and p-JNK1/2 were significantly increased and the expression of Bcl-2 significantly decreased;the drug group and drug control group,compared with the radiation group,the immediate ROS content of cells and the expression of Caspase 3,p53,Bax,p-38MAPK and p-JNK1/2 were significantly decreased and the expression of bcl-2 significantly increased.The results showed that S-HPM radiation could induce oxidative stress damage to GC-2 cells and prophylactic administration of SP could protect HPM radiation damage through antioxidant mechanism.
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