PDF(Pubmed)
Abstract：
UNASSIGNED: Owing to the long penetration depth of gamma (γ)-rays, individuals working in ionizing radiation environments are chronically exposed to low-dose γ-radiation, resulting in cognitive changes. Dose rate significantly affects radiation-induced biological effects; however, its role in chronic low-dose γ-irradiation-induced cognitive impairment remains unclear. We aimed to investigate whether chronic low-dose γ-irradiation at low-dose-rate (LDR) could induce cognitive impairment and to compare the cognitive alteration caused by chronic low-dose γ-irradiation at LDR and high-dose-rate (HDR).
UNASSIGNED: The rats were exposed to γ-irradiation at a LDR of 6 mGy/h and a HDR of 20 mGy/h for 30 days (5 h/day). Functional imaging was performed to assess the brain inflammation and blood-brain barrier (BBB) destruction of rats. Histological and immunofluorescence analyses were used to reveal the neuron damage and the activation of microglia and astrocytes in the hippocampus. RNA sequencing was conducted to investigate changes in gene expression in hippocampus.
UNASSIGNED: The rats in the LDR group exhibited more persistent cognitive impairment than those in the HDR group. Furthermore, irradiated rats showed brain inflammation and a compromised BBB. Histologically, the number of hippocampal neurons were comparable in the LDR group but were markedly decreased in the HDR. Additionally, activated M1-like microglia and A1-like astrocytes were observed in the hippocampus of rats in the LDR group; however, only M1-like microglia were activated in the HDR group. Mechanistically, the PI3K-Akt signaling pathway contributed to the different cognitive function change between the LDR group and HDR group.
UNASSIGNED: Compared with chronic low-dose γ-irradiation at HDR, LDR induced more severe cognitive impairment which might involve PI3K/Akt signaling pathway.
UNASSIGNED: The rats were exposed to γ-irradiation at a LDR of 6 mGy/h and a HDR of 20 mGy/h for 30 days (5 h/day). Functional imaging was performed to assess the brain inflammation and blood-brain barrier (BBB) destruction of rats. Histological and immunofluorescence analyses were used to reveal the neuron damage and the activation of microglia and astrocytes in the hippocampus. RNA sequencing was conducted to investigate changes in gene expression in hippocampus.
UNASSIGNED: The rats in the LDR group exhibited more persistent cognitive impairment than those in the HDR group. Furthermore, irradiated rats showed brain inflammation and a compromised BBB. Histologically, the number of hippocampal neurons were comparable in the LDR group but were markedly decreased in the HDR. Additionally, activated M1-like microglia and A1-like astrocytes were observed in the hippocampus of rats in the LDR group; however, only M1-like microglia were activated in the HDR group. Mechanistically, the PI3K-Akt signaling pathway contributed to the different cognitive function change between the LDR group and HDR group.
UNASSIGNED: Compared with chronic low-dose γ-irradiation at HDR, LDR induced more severe cognitive impairment which might involve PI3K/Akt signaling pathway.
摘要：
■由于伽玛（γ）射线的穿透深度很长，在电离辐射环境中工作的个人长期暴露于低剂量γ辐射，导致认知变化。剂量率显著影响辐射诱导的生物效应；然而，其在慢性低剂量γ射线照射引起的认知障碍中的作用尚不清楚.我们旨在研究低剂量率（LDR）的慢性低剂量γ射线照射是否会引起认知障碍，并比较LDR和高剂量率（HDR）的慢性低剂量γ射线照射引起的认知改变。
将大鼠以6mGy/h的LDR和20mGy/h的HDR暴露于γ-照射30天(5h/天)。进行功能成像以评估大鼠的脑炎症和血脑屏障（BBB）破坏。组织学和免疫荧光分析用于揭示海马中的神经元损伤以及小胶质细胞和星形胶质细胞的激活。进行RNA测序以研究海马中基因表达的变化。
■LDR组的大鼠比HDR组的大鼠表现出更持久的认知障碍。此外，照射的大鼠表现为脑炎症和受损的BBB。组织学上,LDR组海马神经元数量相当,但HDR组海马神经元数量明显减少.此外,LDR组大鼠海马中观察到活化的M1样小胶质细胞和A1样星形胶质细胞；然而，HDR组只有M1样小胶质细胞被激活.机械上,PI3K-Akt信号通路导致LDR组和HDR组之间不同的认知功能变化。
■与HDR下的慢性低剂量γ照射相比，LDR可导致更严重的认知障碍，可能涉及PI3K/Akt信号通路。
将大鼠以6mGy/h的LDR和20mGy/h的HDR暴露于γ-照射30天(5h/天)。进行功能成像以评估大鼠的脑炎症和血脑屏障（BBB）破坏。组织学和免疫荧光分析用于揭示海马中的神经元损伤以及小胶质细胞和星形胶质细胞的激活。进行RNA测序以研究海马中基因表达的变化。
■LDR组的大鼠比HDR组的大鼠表现出更持久的认知障碍。此外，照射的大鼠表现为脑炎症和受损的BBB。组织学上,LDR组海马神经元数量相当,但HDR组海马神经元数量明显减少.此外,LDR组大鼠海马中观察到活化的M1样小胶质细胞和A1样星形胶质细胞；然而，HDR组只有M1样小胶质细胞被激活.机械上,PI3K-Akt信号通路导致LDR组和HDR组之间不同的认知功能变化。
■与HDR下的慢性低剂量γ照射相比，LDR可导致更严重的认知障碍，可能涉及PI3K/Akt信号通路。
