Jingxia Zhao

Nankai University, Tianjin, Tianjin Shi, China

Are you Jingxia Zhao?

Claim your profile

Publications (3)7.48 Total impact

  • Source
    Yinguo Zhang, Jingxia Zhao, Tao Zhang, Zhuo Yang
    [Show abstract] [Hide abstract]
    ABSTRACT: Methylene blue (MB) is a vital dye to allow better visualization and marker of parathyroid glands. The compound causes a toxic encephalopathy in clinical observations and some neuronal adverse effects in experimental studies. Of neurotoxic effects, reduced field excitatory postsynaptic potentials (fEPSPs) in hippocampal slice cultures and apoptosis induced in neurons by MB, suggest that MB may affect electrophysiological properties in neurons. Consequently, studies were undertaken to characterize the effects of MB on voltage-gated sodium currents (I(Na)) in hippocampal CA1 neurons. MB was tested at a clinically-relevant concentration (10μM), of which as a surgical marker of the parathyroid glands, and other concentrations (0.25μM, 1μM, and 100μM). The results showed that MB reduced the amplitude of I(Na) at the concentrations of 10μM and 100μM. No significant changes were found with the other two concentrations of MB. 10μM of MB did not produce a shift in the activation-voltage curve of I(Na) but produced a hyperpolarizing shift in the inactivation-voltage curve of I(Na) and delayed the recovery of I(Na) from inactivation. Action potential (AP) properties and the pattern of repetitive firing were examined using whole-cell current-clamp recordings. Peak amplitude, overshoot and maximum velocity of depolarization (V(max)) of the evoked single AP decreased in the presence of the 10μM MB solution. The rate of repetitive firing also decreased. The results suggest MB as a surgical marker of the parathyroid glands, may cause sodium channel inhibition on neurons in the nervous system.
    NeuroToxicology 12/2010; 31(6):724-9. · 2.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The effects of zinc oxide nanoparticles (nano-ZnO) on the properties of voltage-dependent sodium, potassium currents and evoked action potentials were studied in acutely isolated rat hippocampal CA3 pyramidal neurons at postnatal ages of 10-14 days rats using the whole-cell patch-clamp technique. The results indicated that: (1) in the present of final concentration of 10(-4)g/ml nano-ZnO, the current-voltage curve of sodium current (I(Na)) was decreased, and the peak amplitudes of I(Na) were increased considerably from -50 to +20mV (p<0.05). Meanwhile, the inactivation and the recovery from inactivation of I(Na) were also promoted by the nano-ZnO solution (10(-4)g/ml) (p<0.01). However, the steady-state activation curve of I(Na) was not shifted by the nano-ZnO. (2) The amplitudes of transient outward potassium current (I(A)) were increased by the nano-ZnO solution (10(-4)g/ml), while the current-voltage curve of delayed rectifier potassium current (I(K)) was significantly increased from +20 to +90mV (p<0.05). However, it is apparent that the nano-ZnO solution did not shift the steady-state activation curve of I(A) and I(K), and neither had significant effects on the inactivation and the recovery from inactivation of I(A). (3) Peak amplitude and overshoot of the evoked single action potential were increased and half-width was diminished in the presence of the 10(-4)g/ml nano-ZnO solution (p<0.05). Simultaneously, a prolonged depolarizing current injection enhanced (p<0.05) repetitive firing evoked firing rate. These results suggested that 10(-4)g/ml nano-ZnO solution can lead to an enhancement in the current amplitudes of I(Na) and I(K) by increasing the opening number of sodium channels, delaying rectifier potassium channels, and enhancing the excitability of neurons, which lead to Na(+) influx and the accumulation of intracellular Na(+), as well as K(+) efflux plus the loss of cytoplasmic K(+). These may disturb the ionic homeostasis and the physiological functions of neurons.
    NeuroToxicology 12/2008; 30(2):220-30. · 2.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: This study was to determine the possible neurotoxicity and mechanisms underlying the effects of nano-ZnO with sizes of 20–80 nm on central nervous system (CNS). The cytotoxicity of nano-ZnO was investigated in PC12 cells. The viability of cells was observed by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the generation of reactive oxygen species (ROS) for cells was evaluated by a fluorometry assay. The apoptosis of cells was detected and analyzed by flow cytometry. In addition, effects of nano-ZnO on the properties of high-voltage-activated (HVA) calcium currents were studied in acutely isolated rat hippocampal pyramidal neurons using the whole-cell patch clamp technique. The results of MTT assay showed that nano-ZnO (10−4 g/mL) caused a significant decrease in cell viability (P < 0.05). Nano-ZnO induced intracellular accumulation of ROS and the apoptosis of PC12 cells with the increasing concentration of nano-ZnO in flow cytometric assay (P < 0.05). Further results of electrophysiological recording indicated that 10−4 g/mL nano-ZnO first altered the current–voltage curve and the peak amplitudes of HVA calcium currents at 10 min of the recording, and the peak current amplitudes were increased significantly at the end of 30 min (P < 0.05). All these results suggested that the increase of intracellular ROS was one of potential mechanisms of cellular apoptosis induced by nano-ZnO. Nano-ZnO could cause the elevation of cytosolic calcium levels by enhancement of HVA calcium currents, which would increase the generation of intracellular ROS, and consequently promote the neuronal apoptosis.
    Journal of Nanoparticle Research 14(11). · 2.18 Impact Factor

Publication Stats

47 Citations
7.48 Total Impact Points

Institutions

  • 2008–2010
    • Nankai University
      • Key Laboratory of Bioactive Materials
      Tianjin, Tianjin Shi, China