Peng Xu

Nanjing Medical University, Nanjing, Jiangsu Sheng, China

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Publications (3)5.13 Total impact

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    ABSTRACT: Deoxypodophyllotoxin (DOP) is a natural product that can be isolated from a variety of medicinal herb plants. It is well known for its antitumor, antiviral, and anti-inflammatory activities. However, there are few investigations that address neurotoxic effect of DOP in animal nervous system. In this study, whole-cell patch clamp and calcium imaging techniques were employed to investigate effects of DOP on electrophysiological properties and calcium regulation of rat dorsal root ganglion (DRG) neurons. DOP inhibited both TTX-S (tetrodotoxin-sensitive) and TTX-R (tetrodotoxin-resistant) sodium currents in voltage clamp recording and caused a decrease in the number of action potentials (APs) in current clamp experiment. Suppressive and unfavorable effects of DOP on the kinetics of sodium currents in terms of excitability of DRG neurons may greatly contribute to its antitumor and anti-inflammatory activities. Moreover, DOP evoked increase of intracellular Ca(2+) concentrations ([Ca(2+)](i)) in DRG neurons, and this effect may lead to neuronal cytotoxicity.
    NeuroToxicology 12/2010; 31(6):680-6. · 2.65 Impact Factor
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    ABSTRACT: to investigate the effect of deoxypodophyllotoxin (DOP) on membrane potential of dorsal unpaired median neurons (DUM, neurons) and its correlation with sodium channel. DUM neurons were labeled with DiBAC4(3). Laser scanning confocal microscope was used to monitor the changes of membrane potential at real time on these neurons that were treated with different concentrations of the DOP. The effect of sodium channel blocker tetrodotoxin (TTX) on the changes was also observed. membrane potential depolarization induced by the DOP peaked at 5 min and became stabilized after 8min. After compared with fluorescence intensity without treatment, the normalized fluorescence intensity was 69.6 ± 3.0, 72.1 ± 2.7, 77.8 ± 3.6, 86.2 ± 3.1 in cells which were treated with 1, 5, 25, 125 micromol/L DOP, respectively. These numbers were significantly lower than those from untreated control cells (P < 0.01). When DUM neurons were co-incubated with 1 micromol/L TTX for 20 min, then treated with 25 micromol/L DOP, the intensity changed to 63.6 ± 5.4, which was similar to that of the control (P > 0.05). This indicated that the effect of DOP could be completely inhibited by TTX. DOP induced membrane depolarization of DUM neurons in the range of 1 approximately 125 micromol/L and the sodium channel should be involved in this process.
    Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 10/2010; 28(10):740-3.
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    ABSTRACT: Low voltage-activated, rapidly inactivating T-type Ca2+ channels are found in a variety of cells, where they regulate electrical activity and Ca2+ entry. In whole-cell patch-clamp recordings from mouse spermatogenic cells, trace element copper (Cu2+) inhibited T-type Ca2+ current (IT-Ca) with IC50 of 12.06 microM. Inhibition of IT-Ca by Cu2+ was concentration-dependent and mildly voltage-dependent. When voltage stepped to -20 mV, Cu2+ (10 microM) inhibited IT-Ca by 49.6 +/- 4.1%. Inhibition of IT-Ca by Cu2+ was accompanied by a shift of -2.23 mV in the voltage dependence of steady-state inactivation. Cu2+ upshifted the current-voltage (I-V) curve. To know the change of the gating kinetics of T-type Ca2+ channels, we analyzed the effect of Cu2+ on activation, inactivation, deactivation and reactivation of T-type Ca2+ channels. Since T-type Ca2+ channels are a key component in capacitation and the acrosome reaction, our data suggest that Cu2+ can affect male reproductive function through T-type Ca2+ channels as a preconception contraceptive material.
    Journal of Membrane Biology 02/2009; 227(2):87-94. · 2.48 Impact Factor

Publication Stats

5 Citations
5.13 Total Impact Points

Institutions

  • 2010
    • Nanjing Medical University
      • Key Laboratory of Modern Toxicology (MOE)
      Nanjing, Jiangsu Sheng, China