The prevalence of domestic and industrial electrical appliances has raised concerns about the health risk of extremely low-frequency magnetic fields（ELF-MFs）. At present, the effects of ELF-MFs on the central nervou...The prevalence of domestic and industrial electrical appliances has raised concerns about the health risk of extremely low-frequency magnetic fields（ELF-MFs）. At present, the effects of ELF-MFs on the central nervous system are still highly controversial, and few studies have investigated its effects on cultured neurons. Here, we evaluated the biological effects of different patterns of ELF-MF exposure on primary cultured hippocampal neurons in terms of viability, apoptosis, genomic instability,and oxidative stress. The results showed that repeated exposure to 50-Hz 2-mT ELF-MF for 8 h per day after different times in culture decreased the viability and increased the production of intracellular reactive oxidative species in hippocampal neurons. The mechanism was potentially related to the up-regulation of Nox2 expression.Moreover, none of the repeated exposure patterns had significant effects on DNA damage, apoptosis, or autophagy, which suggested that ELF-MF exposure has no severe biological consequences in cultured hippocampal neurons.展开更多
Magnesium （Mg）-based biomaterials have shown great potential in clinical applications. However, the cytotoxic effects of excessive Mg2. and the corrosion products from Mg-based biomaterials, particularly their effec...Magnesium （Mg）-based biomaterials have shown great potential in clinical applications. However, the cytotoxic effects of excessive Mg2. and the corrosion products from Mg-based biomaterials, particularly their effects on neurons, have been little studied. Although viability tests are most commonly used, a functional evaluation is critically needed. Here, both methyl thiazolyl tetrazolium （MTT） and lactate de- hydrogenase （LDH） assays were used to test the effect of Mg2. and Mg-extract solution on neuronal viability. Microelectrode arrays （MEAs）, which provide long-term, real-time recording of extracellular electro- physiological signals of in vitro neuronal networks, were used to test for toxic effects. The minimum effective concentrations （ECmin） of Mg2. from the MTr and LDH assays were 3 mmol/L and 100 mmol/L respec- tively, while the ECmin obtained from the MEA assay was 0.1 mmol/L MEA data revealed significant loss of neuronal network activity when the culture was exposed to 25% Mg-extract solution, a concentra- tion that did not affect neuronal viability. For evaluating the biocompatibility of Mg-based biomaterials with neurons, MEA electrophysiological testing is a more precise method than basic cell-viability testing.展开更多
Indirubin-3′-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer＇s disease. Here, we found that indirubin-3′-monoxime improved th...Indirubin-3′-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer＇s disease. Here, we found that indirubin-3′-monoxime improved the morphology and increased the survival rate of SHSY5 Y cells exposed to amyloid-beta 25–35（Aβ25–35）, and also suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205. Furthermore, indirubin-3′-monoxime inhibited phosphorylation of glycogen synthase kinase-3β（GSK-3β）. Our results suggest that indirubin-3′-monoxime reduced Aβ25–35-induced apoptosis by suppressing tau hyperphosphorylation via a GSK-3β-mediated mechanism. Indirubin-3′-monoxime is a promising drug candidate for Alzheimer＇s disease.展开更多
The present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransm...The present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 μM arsenite for 24 hours. Cell viability and morphological observations revealed that 5 μM arsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 μM arsenite for 24 hours and stimulated with 25 μM glutamate for 10 minutes. Results showed that [Ca2＋]i in astrocytes exposed to 5 and 10 μM arsenite was significantly increased and levels of D-serine, γ-aminobutyric acid and glycine in cultures exposed to 2.5-10 μM arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 μM arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function.展开更多
Different outcomes of astrocyte inflammatory signalling in injury and neurodegeneration：It is emerging that astrocytes have a significant impact on the neuronal network by modulating synaptic connections and neuronal...Different outcomes of astrocyte inflammatory signalling in injury and neurodegeneration：It is emerging that astrocytes have a significant impact on the neuronal network by modulating synaptic connections and neuronal viability in both normal and pathological states.展开更多
基金supported by the National Natural Science Foundation(31170799 and 30872082)the National Basic Research Development Program(973 Program)of China(2011CB503702)
文摘The prevalence of domestic and industrial electrical appliances has raised concerns about the health risk of extremely low-frequency magnetic fields（ELF-MFs）. At present, the effects of ELF-MFs on the central nervous system are still highly controversial, and few studies have investigated its effects on cultured neurons. Here, we evaluated the biological effects of different patterns of ELF-MF exposure on primary cultured hippocampal neurons in terms of viability, apoptosis, genomic instability,and oxidative stress. The results showed that repeated exposure to 50-Hz 2-mT ELF-MF for 8 h per day after different times in culture decreased the viability and increased the production of intracellular reactive oxidative species in hippocampal neurons. The mechanism was potentially related to the up-regulation of Nox2 expression.Moreover, none of the repeated exposure patterns had significant effects on DNA damage, apoptosis, or autophagy, which suggested that ELF-MF exposure has no severe biological consequences in cultured hippocampal neurons.
基金supported by the National Basic Research Program of China (973 Program,No.2012CB619102)the National Natural Science Foundation of China (Nos.31070847 and 31370956)+3 种基金the National Science and Technology Support Program (No.2012BAI18B01)the Strategic New Industry Development Special Foundation of Shenzhen,China (No.JCYJ20130402172114948)the Guangdong Provincial Department of Science and Technology,China (No.2011B050400011)NIH NIGMS COBRE (No.NIH P20GM103444)
文摘Magnesium （Mg）-based biomaterials have shown great potential in clinical applications. However, the cytotoxic effects of excessive Mg2. and the corrosion products from Mg-based biomaterials, particularly their effects on neurons, have been little studied. Although viability tests are most commonly used, a functional evaluation is critically needed. Here, both methyl thiazolyl tetrazolium （MTT） and lactate de- hydrogenase （LDH） assays were used to test the effect of Mg2. and Mg-extract solution on neuronal viability. Microelectrode arrays （MEAs）, which provide long-term, real-time recording of extracellular electro- physiological signals of in vitro neuronal networks, were used to test for toxic effects. The minimum effective concentrations （ECmin） of Mg2. from the MTr and LDH assays were 3 mmol/L and 100 mmol/L respec- tively, while the ECmin obtained from the MEA assay was 0.1 mmol/L MEA data revealed significant loss of neuronal network activity when the culture was exposed to 25% Mg-extract solution, a concentra- tion that did not affect neuronal viability. For evaluating the biocompatibility of Mg-based biomaterials with neurons, MEA electrophysiological testing is a more precise method than basic cell-viability testing.
基金supported by the Nanjing Medical Science and Technique Development Foundation of China,No.QRX11199a grant from the Nanjing Science and Technology Commission Project of China,No.201303010a grant from the Health Research Project in Nanjing City of China,No.YKK14101
文摘Indirubin-3′-monoxime is an effective inhibitor of cyclin-dependent protein kinases, and may play an obligate role in neuronal apoptosis in Alzheimer＇s disease. Here, we found that indirubin-3′-monoxime improved the morphology and increased the survival rate of SHSY5 Y cells exposed to amyloid-beta 25–35（Aβ25–35）, and also suppressed apoptosis by reducing tau phosphorylation at Ser199 and Thr205. Furthermore, indirubin-3′-monoxime inhibited phosphorylation of glycogen synthase kinase-3β（GSK-3β）. Our results suggest that indirubin-3′-monoxime reduced Aβ25–35-induced apoptosis by suppressing tau hyperphosphorylation via a GSK-3β-mediated mechanism. Indirubin-3′-monoxime is a promising drug candidate for Alzheimer＇s disease.
基金supported by the National Natural Science Foundation of China,No.30972441,81202158
文摘The present study used cultures of primary astrocytes, isolated from neonatal rats, to verify the hypothesis that arsenite-induced neurotoxicity can influence neuronal function by altering glutamate-induced gliotransmitter release. Primary astrocytes were exposed to 0, 2.5, 5, 10, 20 or 30 μM arsenite for 24 hours. Cell viability and morphological observations revealed that 5 μM arsenic exposure could induce cytotoxicity. Cells were then cultured in the presence of 0, 2.5, 5, or 10 μM arsenite for 24 hours and stimulated with 25 μM glutamate for 10 minutes. Results showed that [Ca2＋]i in astrocytes exposed to 5 and 10 μM arsenite was significantly increased and levels of D-serine, γ-aminobutyric acid and glycine in cultures exposed to 2.5-10 μM arsenite were also increased. However, glutamate levels in the media were significantly increased only after treatment with 10 μM arsenite. In conclusion, our findings suggest that arsenic exposure may affect glutamate-induced gliotransmitter release from astrocytes and further disturb neuronal function.
文摘Different outcomes of astrocyte inflammatory signalling in injury and neurodegeneration：It is emerging that astrocytes have a significant impact on the neuronal network by modulating synaptic connections and neuronal viability in both normal and pathological states.
