-
[show abstract]
[hide abstract]
ABSTRACT: Tau protein, a microtubule-associated protein involved in a number of neurological disorders such as Alzheimer's disease (AD), may undergo modifications under both physiological and pathological conditions. However, the signaling pathways that couple tau protein to neuronal physiology such as synaptic plasticity have not yet been elucidated. Here we report that tau protein is involved in morphological plasticity in response to brain derived neurotrophic factor (BDNF). Stimulation of the cultured rat hippocampal neurons with BDNF resulted in increased tau protein expression, as detected by Western blotting. Furthermore, tau protein accumulated in the distal region of the neurite when treated with taxol or taxol plus BDNF. The increased tau protein also protected neurons against nocodazole-induced dendrite loss. Moreover, BDNF promoted spine growth as well as tau protein over-expression. Knockdown of tau protein using specific short-hairpin RNA (shRNA) significantly decreased the spine density. And BDNF could not increase the spine density of tau-knockdown neurons. These results highlight a possible role for tau protein in the dynamic rearrangement of cytoskeletal fibers vital for BDNF-induced synaptic plasticity.
Neurochemistry International 02/2012; 60(3):233-42. · 2.86 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Recent studies suggest that oxidative stress and mitochondrial dysfunction play important roles in the neurotoxicity of nickel. Because mitochondrial DNA (mtDNA) is highly vulnerable to oxidative stress and melatonin can efficiently protect mtDNA against oxidative damage in various pathological conditions, the aims of this study were to determine whether mtDNA oxidative damage was involved in the neurotoxicity of nickel and to assay the neuroprotective effects of melatonin in mtDNA. In this study, we exposed mouse neuroblastoma cell lines (Neuro2a) to different concentrations of nickel chloride (NiCl(2), 0.125, 0.25, and 0.5 mm) for 24 hr. We found that nickel significantly increased reactive oxygen species (ROS) production and mitochondrial superoxide levels. In addition, nickel exposure increased mitochondrial 8-hydroxyguanine (8-OHdG) content and reduced mtDNA content and mtDNA transcript levels. Consistent with this finding, nickel was found to destroy mtDNA nucleoid structure and decrease protein levels of Tfam, a key protein component for nucleoid organization. However, all the oxidative damage to mtDNA induced by nickel was efficiently attenuated by melatonin pretreatment. Our results suggest that oxidative damage to mtDNA may account for the neurotoxicity of nickel. Melatonin has great pharmacological potential in protecting mtDNA against the adverse effects of nickel in the nervous system.
Journal of Pineal Research 05/2011; 51(4):426-33. · 5.79 Impact Factor
-
Min-Di He,
Shang-Cheng Xu,
Yong-Hui Lu,
Li Li,
Min Zhong, Yan-Wen Zhang,
Yuan Wang,
Min Li,
Ju Yang,
Guang-Bin Zhang,
Zheng-Ping Yu,
Zhou Zhou
[show abstract]
[hide abstract]
ABSTRACT: Mitochondrial dysfunction is thought to be a part of the mechanism underlying nickel-induced neurotoxicity. L-carnitine (LC), a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine in all mammalian species, manifests its neuroprotective effects by improving mitochondrial energetics and function. The purpose of this study was to investigate whether LC could efficiently protect against nickel-induced neurotoxicity. Here, we exposed a mouse neuroblastoma cell line (Neuro-2a) to different concentrations of nickel chloride (NiCl₂) (0.25, 0.5, 1, and 2 mM) for 24 h, or to 0.5 mM and 1 mM NiCl₂ for various periods (0, 3, 6, 12, or 24 h). We found that nickel significantly increased the cell viability loss and lactate dehydrogenase (LDH) release in Neuro-2a cells. In addition, nickel exposure significantly elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, disrupted the mitochondrial membrane potential (ΔΨ(m)), reduced adenosine-5'-triphosphate (ATP) concentrations and decreased mitochondrial DNA (mtDNA) copy numbers and mtRNA transcript levels. However, all of the cytotoxicities and mitochondrial dysfunctions that were triggered by nickel were efficiently attenuated by pretreatment with LC. These protective effects of LC may be attributable to its role in maintaining mitochondrial function in nickel-treated cells. Our results suggest that LC may have great pharmacological potential in protecting against the adverse effects of nickel in the nervous system.
Toxicology and Applied Pharmacology 03/2011; 253(1):38-44. · 4.45 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Nickel is a potential neurotoxic pollutant. Oxidative stress is supposed to be involved in the mechanism underlying nickel-induced neurotoxicity. Melatonin has efficient protective effects against various oxidative damages in nervous system. The purpose of this study was to investigate whether melatonin could efficiently protect against neurotoxicity induced by nickel. Here, we exposed primary cultured cortical neurons and mouse neuroblastoma cell lines (neuro2a) to different concentrations of nickel chloride (NiCl(2)) (0.125, 0.25, 0.5, and 1 mm) for 12 hr or 0.5 mm NiCl(2) for various periods (0, 3, 6, 12, and 24 hr). We found that nickel significantly increased reactive oxygen species production and caused the loss of cell viability both in cortical neurons and neuro2a cells. In addition, nickel exposure obviously inhibited the mitochondrial function, disrupted the mitochondrial membrane potential (DeltaPsim), reduced ATP production, and decreased mitochondrial DNA (mtDNA) content. However, each of these oxidative damages was efficiently attenuated by melatonin pretreatment. These protective effects of melatonin may be attributable to its roles in reducing oxidative stress and improving mitochondrial function in nickel-treated nerve cells. Our results suggested that melatonin may have great pharmacological potential in protecting against the adverse effects of nickel in the nervous system.
Journal of Pineal Research 08/2010; 49(1):86-94. · 5.79 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Our previous investigation indicated that electromagnetic radiation level of city environment in some frequency range has gotten close to national standard limits. This study is to investigate the effects of these frequency electromagnetic waves coexisted in same environment on teenagers' electrocardiogram and blood cells.
Electrocardiogram and blood cells were examined in 106 cases of teenagers by using electrocardiograph and blood counting instruments respectively.
There were not significantly different in heart rate, P-R interphase, QRS-wave time, Q-T interphase, blood hemoglobin content and blood platelet number in teenagers between high and low electromagnetic radiation environment (P > 0.05). The total blood leucocyte number in teenagers was statistically lower in high electromagnetic radiation environment than that in low electromagnetic radiation environment (P < 0.05). With regard to classification of blood leucocyte, the blood monocyte number in 14 - 18 years old of teenagers and the blood eosinophil number in boy were significantly higher in high electromagnetic radiation environment than those in low electromagnetic radiationenvironment (P < 0.05).
The electromagnetic radiation nowadays in metropolis environment may have no harmful effects on teenagers' electrocardiogram and have harmful effects on teenagers' blood leucocyte-mainly showing decreased total blood leucocyte number, increased percentages of monocyte and eosinophil number.
Wei sheng yan jiu = Journal of hygiene research 01/2005; 34(1):43-5.
-
[show abstract]
[hide abstract]
ABSTRACT: A novel chalcone derivative was isolated from Onychium japonicum and its structure was elucidated by spectroscopic methods. The isolated compound showed cytotoxic activity against the human carcinoma cell lines Hela and BEL-7402 in vitro.
Chinese Chemical Letters.
