Corticosterone, a principal glucocorticoid synthesized in the rodent adrenal cortex, can be cumula- tively toxic to hippocampal neurons, the cause of which is not known. The present study determined whether the cytoso...Corticosterone, a principal glucocorticoid synthesized in the rodent adrenal cortex, can be cumula- tively toxic to hippocampal neurons, the cause of which is not known. The present study determined whether the cytosol adenylate kinase （AK） system long-term exposure to high corticosterone levels. We was involved in the neuronal damage induced by nvestigated the effects of long-term exposure to high corticosterone levels on AK1 activity, AK1 mRNA expression, and energy levels in cultured hippocampal neurons. The results show that long-term exposure to high corticosterone levels induces a reduction of the cultured hippocampal neuron viability, significantly reduces energy levels, and causes a time-dependant re- duction of the AK1 activity. These findings indicate that changes in the AK system might be the mechanism underlying neuronal damage induced by long-term exposure to high corticosterone levels.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
目的:MMP(髓鞘膜蛋白)减低新生神经元的活力的现象可以被黄芪纠正。然而,新生神经元与成年神经元具有不同的生理特性。因此,研究黄芪能否改善成年神经元的活力有重要意义。方法:用MTT(四甲基偶氮唑盐)实验检测体外培养的,并用MMP,NGF,Ra...目的:MMP(髓鞘膜蛋白)减低新生神经元的活力的现象可以被黄芪纠正。然而,新生神经元与成年神经元具有不同的生理特性。因此,研究黄芪能否改善成年神经元的活力有重要意义。方法:用MTT(四甲基偶氮唑盐)实验检测体外培养的,并用MMP,NGF,Rad ix Astragali,NGF+MMP,Rad ix Astragali+MMP处理的各组成年大鼠脑皮层神经元的细胞活力。结果:MMP组的细胞活力明显低于对照组(未加任何药物组),而黄芪、NGF、NGF+MMP以及黄芪+MMP组之间,神经元的活力无显著性差异。结论:黄芪可以改善MMP减低的成年皮层神经元的活力。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
基金Supported by the National Natural Science Foundation of China (No. 90713043)the Specialized Research Fund for Doctoral Program of Higher Education of MOE, P.R.C. (No. 20060003072)+1 种基金the Key Technologies Research and Development Program of the 11th Five-Year Plan of China (No. 2006BAIO8B03-09)the Fund for Basic Research from the Nanjing University of Traditional Chinese Medicine (No. 08XJC02)
文摘Corticosterone, a principal glucocorticoid synthesized in the rodent adrenal cortex, can be cumula- tively toxic to hippocampal neurons, the cause of which is not known. The present study determined whether the cytosol adenylate kinase （AK） system long-term exposure to high corticosterone levels. We was involved in the neuronal damage induced by nvestigated the effects of long-term exposure to high corticosterone levels on AK1 activity, AK1 mRNA expression, and energy levels in cultured hippocampal neurons. The results show that long-term exposure to high corticosterone levels induces a reduction of the cultured hippocampal neuron viability, significantly reduces energy levels, and causes a time-dependant re- duction of the AK1 activity. These findings indicate that changes in the AK system might be the mechanism underlying neuronal damage induced by long-term exposure to high corticosterone levels.
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.
文摘目的:MMP(髓鞘膜蛋白)减低新生神经元的活力的现象可以被黄芪纠正。然而,新生神经元与成年神经元具有不同的生理特性。因此,研究黄芪能否改善成年神经元的活力有重要意义。方法:用MTT(四甲基偶氮唑盐)实验检测体外培养的,并用MMP,NGF,Rad ix Astragali,NGF+MMP,Rad ix Astragali+MMP处理的各组成年大鼠脑皮层神经元的细胞活力。结果:MMP组的细胞活力明显低于对照组(未加任何药物组),而黄芪、NGF、NGF+MMP以及黄芪+MMP组之间,神经元的活力无显著性差异。结论:黄芪可以改善MMP减低的成年皮层神经元的活力。
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.
