[논문]Effects of combined radiofrequency field exposure on amyloid-beta–induced cytotoxicity in HT22 mouse hippocampal neurones

Lee, Jong-Sun; Kim, Jeong-Yub; Kim, Hee-Jin; Kim, Jeong Cheol; Lee, Jae-Seon; Kim, Nam; Park, Myung-Jin

doi:10.1093/jrr/rrw040

Effects of combined radiofrequency field exposure on amyloid-beta–induced cytotoxicity in HT22 mouse hippocampal neurones 원문보기

Journal of radiation research, v.57 no.6, 2016년, pp.620 - 626

Lee, Jong-Sun (Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences , Nowongil 75 , Nowon-Gu , Seoul 139-706 , Korea) , Kim, Jeong-Yub (Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences , Nowongil 75 , Nowon-Gu , Seoul 139-706 , Korea) , Kim, Hee-Jin (Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences , Nowongil 75 , Nowon-Gu , Seoul 139-706 , Korea) , Kim, Jeong Cheol (Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences , Nowongil 75 , Nowon-Gu , Seoul 139-706 , Korea) , Lee, Jae-Seon (Division of Biomedical Sciences , College of Medicine , Inha University , Incheon 400-712 , Korea) , Kim, Nam (School of Information and Communication Engine) , Park, Myung-Jin

Abstract ▼ AI-Helper

Alzheimer's disease (AD) is the most common progressive and irreversible neurodegenerative disease and it is caused by neuronal death in the brain. Recent studies have shown that non-ionizing radiofrequency (RF) radiation has some beneficial cognitive effects in animal models of AD. In this study, we examined the effect of combined RF radiation on amyloid-beta (Aβ)–induced cytotoxicity in HT22 rat hippocampal neurons. Treatment with Aβ suppressed HT22 cell proliferation in a concentration-dependent manner. RF exposure did not affect cell proliferation, and also had a marginal effect on Aβ-induced suppression of growth in HT22 cells. Cell cycle analysis showed that Aβ decreased the G1 fraction and increased the subG1 fraction, indicating increased apoptosis. Accordingly, Aβ increased the annexin V/propidium iodide (PI)–positive cell fraction and the degradation of poly (ADP ribose) polymerase and caspase-3 in HT22 cells. However, RF alone and the combination of Aβ and RF did not affect these events significantly. Aβ increased reactive oxygen species (ROS) generation, thereby suppressing cell proliferation. This was abrogated by N-acetylcysteine (NAC) treatment, indicating that Aβ-induced ROS generation is the main cause of suppression of proliferation. NAC also restored Aβ-induced annexin V/PI–positive cell populations. However, RF did not have a significant impact on these events. Finally, Aβ stimulated the ataxia telangiectasia and Rad3-related protein/checkpoint kinase 1 DNA single-strand breakage pathway, and enhanced beta-site amyloid precursor protein expression; RF had no effect on them. Taken together, our results demonstrate that RF exposure did not significantly affect the Aβ-induced decrease of cell proliferation, increase of ROS production, or induction of cell death in these cells.

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참고문헌 (15)

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Effects of combined radiofrequency field exposure on amyloid-beta–induced cytotoxicity in HT22 mouse hippocampal neurones 원문보기

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Effects of combined radiofrequency field exposure on amyloid-beta–induced cytotoxicity in HT22 mouse hippocampal neurones 원문보기

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