Li Jianguo, Zhang Guowei, Meng Zhuangzhi, Wang Lingzhan, Liu Haiying, Liu Qiang, Buren Batu
Laboratory of Biomedicine, Department of Hemopathic Tumor of Mongolian Medicine, The Affiliated Hospital of Inner Mongolia University for The Nationalities, Neimenggu Tongliao, Inner Mongolia 028007, P.R. China; Tianjin Key Laboratory of Molecular Nuclear Medicine, Institute of Radiation Medicine, Chinese Academy of Medical Science and Peking Union Medical College, Tianjin 300192, P.R. China; Department of Human Anatomy, The School of Medicine of Inner Mongolia University for The Nationalities, Neimenggu Tongliao, Inner Mongolia 028007, P.R. China.
Department of Human Anatomy, The School of Medicine of Inner Mongolia University for The Nationalities, Neimenggu Tongliao, Inner Mongolia 028007, P.R. China.
Exp Ther Med. 2016 Jun;11(6):2385-2390. doi: 10.3892/etm.2016.3215. Epub 2016 Mar 31.
Neuronal cell apoptosis is associated with various factors that induce neurological damage, including radiation exposure. When administered prior to exposure to radiation, a protective agent may prevent cellular and molecular injury. The present study aimed to investigate whether melatonin exerts a neuroprotective effect by inhibiting the caspase cell death pathway. Male Sprague-Dawley rats were administered melatonin (100 mg/kg body weight) 30 min prior to radiation exposure in red light during the evening. In order to elucidate whether melatonin has a neuroprotective role, immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick-end labeling, Nissl staining, reverse transcription-quantitative polymerase chain reaction, reactive oxygen species analysis and western blotting were performed. At 24 h post-melatonin treatment, caspase-3 mRNA and protein expression levels were significantly decreased. These results demonstrated that melatonin may protect hippocampal neurons via the inhibition of caspase-3 when exposed to irradiation. Therefore, caspase-3 inhibition serves a neuroprotective and antioxidant role in the interventional treatment of melatonin. The results of the present study suggested that melatonin may have a potential therapeutic effect against irradiation; however, further studies are required in order to elucidate the underlying antioxidant mechanisms.
神经元细胞凋亡与多种诱导神经损伤的因素有关，包括辐射暴露。在辐射暴露前给予一种保护剂可能会预防细胞和分子损伤。本研究旨在探讨褪黑素是否通过抑制半胱天冬酶细胞死亡途径发挥神经保护作用。在傍晚红光下，雄性Sprague-Dawley大鼠在辐射暴露前30分钟给予褪黑素（100毫克/千克体重）。为了阐明褪黑素是否具有神经保护作用，进行了免疫组织化学、末端脱氧核苷酸转移酶dUTP缺口末端标记、尼氏染色、逆转录-定量聚合酶链反应、活性氧分析和蛋白质印迹法。在褪黑素治疗后24小时，半胱天冬酶-3的mRNA和蛋白表达水平显著降低。这些结果表明，褪黑素在暴露于辐射时可能通过抑制半胱天冬酶-3来保护海马神经元。因此，抑制半胱天冬酶-3在褪黑素的介入治疗中起到神经保护和抗氧化作用。本研究结果表明，褪黑素可能对辐射具有潜在的治疗作用；然而，需要进一步研究以阐明潜在的抗氧化机制。
