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Objective:To study the therapeutic effect Tetrandrine (TET) on striatal injury caused by microwave radiation and underlying mechanism.Methods:C57BL/6N mice were randomly divided into blank control group (C), radiation control group (R), TET group (TET) and TET combined with radiation group (TET+ R). The mice of radiation group were exposed to 2.856 GHz 8 mW/cm2 microwave on whole-body for 15 min. TET (60 mg/kg) was injected intraperitoneally once a day for 3 consecutive days. The TET structure was verified by ultraviolet spectrophotometry. The open field experiment was used to detect the change of anxiety in mice. Histopathological and ultrastructural changes of the striatum were observed by light microscopy and transmission electron microscopy (TMT). Quantitative real-time PCR (qPCR) was used to detect gene expression changes of voltage-gated calcium channel (VGCC) subtype in the striatum.Results:The open field experiments showed that the time and distance of mice to explore the central region after microwave radiation were significantly lower than that before radiation ( t=4.60, 5.18, P<0.01), and the TET administration significantly improved these changes ( F=1.43, 4.37, P < 0.05). 7 d after microwave radiation, some neuronal nuclei in the striatum of mice contracted and could be stained deeply, which was more obvious in the globus pallidus area. The partial neuronal apoptosis, swelling and cavitation of glial cell mitochondria, blurring of synaptic gaps, and widening of perivascular gaps in the striatum were observed by TMT. The above lesions were significantly rescued after TET administration. But both microwave radiation and TET administration had no significant effect on the gene expressions of striatal VGCC ( P > 0.05). Conclusions:TET has a therapeutic effect on anxiety-like behavior and structural damage of striatum caused by microwave radiation, which is independent of the expression of striatal VGCC genes.
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Objective:To investigate the effects of microwave radiation on associative learning and memory function and hippocampal structure of mice.Methods:C57BL/6N mice were ramdomly divided into sham-radiated group ( n=27) and radiation group ( n=2). The radiation group was exposed to microwave at 2.856 GHz, 8 mW/cm 2 for 15 min, then their spatial and associative learning and memory function were examined with the morris water maze and shuttle box behavior experiment. The pathological changes of hippocampal tissue were observed by HE staining and light microscope, the ultrastructural changes of hippocampal tissue were observed by transmission electron microscope. Results:After microwave radiation, the times of mice crossing the platform for the reverse space exploration decreased from(3.60±0.79) times to (2.55±0.47) times( t=2.21, P=0.046), the average active escape rate decreased significantly ( t = 2.70, P<0.05), and the average active latency and the total shock time was significantly prolonged ( t = -3.09, -3.02, P < 0.05). At 8 d after microwave radiation, the nuclei of some neurons in the CA3 and DG regions of the hippocampus were pyknosis. The neurons were apoptotic, the synaptic spaces blurred, the glial cells swollen, and the perivascular spaces widened in the CA3 region of the hippocampus. Conclusions:Microwave radiation can decline the spatial reference memory ability and associative learning and memory ability of mice. The morphological and pathological changes of hippocampus are the structural basis of this dysfunction.
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In this study, fifty-four male Wistar rats were randomly divided into four groups according to the static magnetic field (SMF) intensity, namely, control, low-intensity, moderate-intensity, and high-intensity groups. The rats' whole body was exposed to a superconducting magnet exposure source. The exposure SMF intensity for the low-intensity, moderate-intensity, and high-intensity groups was 50 m T, 100 m T, and 200 m T, respectively, and the exposure time was 1 h/day for consecutive 15 days. After different exposure times, glucose metabolism in rats' brain was evaluated by micro-positron emission tomography (micro-PET), and the expression of hexokinase 1(HK1) and 6-phosphate fructokinase-1(PFK1) was detected by western blot. The exploration and locomotion abilities of the rats were evaluated by conducting open field test (OFT). Furthermore, pathological changes of rats' brain were observed under a microscope by using hematoxylin-eosin staining. PET results showed that moderate-intensity SMFs could cause fluctuant changes in glucose metabolism in rats' brain and the abnormalities were SMF intensity dependent. The expression of the two rate-limiting enzymes HK1 and PFK1 in glucose metabolism in brain significantly decreased after SMF exposure. The OFT showed that the total distance, surrounding distance, activity time, and climbing and standing times significantly decreased after SMF exposure. The main pathological changes in the brain were pyknosis, edema of neurons, and slight widening of the perivascular space, which occurred after 15 times of exposure. This study indicated that SMF exposure could lead to abnormal glucose metabolism in the brain and might result in anxiety-like behaviors.
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Ansiedad/metabolismo , Encéfalo/metabolismo , Glucosa/metabolismo , Campos Magnéticos , Animales , Ansiedad/diagnóstico por imagen , Encéfalo/diagnóstico por imagen , Hexoquinasa/metabolismo , Masculino , Fosfofructoquinasa-1/metabolismo , Tomografía de Emisión de Positrones , Ratas , Ratas WistarRESUMEN
Large artery atherosclerosis and the vascular stenosis caused by it are the important causes of ischemic stroke. Cerebral microbleeds are an imaging manifestation of cerebral small vessel disease. Intracranial large blood vessels and small blood vessels are structurally continuous, simultaneously affected by hemodynamics, and exposed to overlapping risk factors, so both of them may coexist in the same organism. This article reviews the research progress of the relationship between large artery atherosclerosis and cerebral microbleeds in recent years.