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Zhao-Bing Gao

Publications and source records attributed to Zhao-Bing Gao.

3 recordsLinked to original sources

Discovering potassium channel blockers from synthetic compound database by using structure-based virtual screening in conjunction with electrophysiological assay.

Potassium ion (K+) channels are attractive targets for drug discovery because of the essential roles played in biological systems. However, high-throughput screening (HTS) cannot be used to screen K+ channel blockers. To overcome this disadvantage of HTS, we have developed a virtual screening approach for discovering novel blockers of K+ channels. On the basis of a three-dimensional model of the eukaryotic K+ channels, molecular docking-based virtual screening was employed to search the chemical database MDL Available Chemicals Directory (ACD). Compounds were ranked according to their relative binding energy, favorable shape complementarity, and potential to form hydrogen bonds with the outer mouth of the K+ channel model. Twenty candidate compounds selected from the virtual screening were examined using the whole-cell voltage-clamp recording in rat dissociated hippocampal neurons. Among them, six compounds (5, 6, 8, 18-20) potently blocked both the delayed rectifier (IK) and fast transient K+ currents (IA). When applied externally, these six compounds preferentially blocked IK with potencies 2- to 500-fold higher than that of tetraethylammonium chloride. Intracellular application of the six compounds had no effect on both K+ currents. In addition, the interaction models and binding free energy calculations demonstrated that hydrophobic interaction and solvent effects play important roles in the inhibitory activities of these compounds. The results demonstrated that structure-based computer screening strategy could be used to identify novel, structurally diverse compounds targeting the pore binding pocket of the outer mouth of voltage-gated K+ channels. This study provides an alternative way of finding new blockers of voltage-gated K+ channels, while the techniques for high-throughput screening of K+ channel drugs remain in development.

Animals↗

Inhibition of excitatory synaptic transmission by trans-resveratrol in rat hippocampus.

The red wine polyphenol trans-resveratrol has been found to exert potent protective actions in a variety of cerebral ischemia models. The neuroprotection by trans-resveratrol thus far is mainly attributed to its intrinsic antioxidant properties. In the present study, the effects of the red wine polyphenol on excitatory synaptic transmission were investigated in the CA1 region of rat hippocampal slices. Perfusion with trans-resveratrol (10-100 microM) caused a concentration-dependent inhibition on the filed excitatory postsynaptic potentials (the field EPSPs) without detectable effect on the presynaptic volleys. The inhibition had a slow onset and was reversible. Trans-resveratrol (30 microM) did not change the ratios of paired-pulse facilitation of the field EPSPs tested at intervals of 20, 40 and 80 ms, nor did it alter the membrane properties of postsynaptic CA1 pyramidal neurons. However, trans-resveratrol (30 microM) significantly suppressed glutamate-induced currents in postsynaptic CA1 pyramidal neurons. In dissociated hippocampal neurons, the IC(50) value of trans-resveratrol in inhibition of glutamate-induced currents was 53.3+/-9.4 microM. Kainite and NMDA receptors were more sensitive to the red wine polyphenol than AMPA receptors. The present study for the first time demonstrates that trans-resveratrol inhibits the postsynaptic glutamate receptors, which probably works in concert with its antioxidant action for ameliorating the brain ischemic injury. The findings also support the future use of trans-resveratrol in the treatment of various neurodegenerative disorders.

Animals↗

Trans-resveratrol, a red wine ingredient, inhibits voltage-activated potassium currents in rat hippocampal neurons.

The red wine ingredient trans-resveratrol was found to exert potent neuroprotective effects in different in vivo and in vitro models. Thus far, the mechanisms underlying the neuroprotection were attributed mainly to its antioxidant properties. The aim of this study was to investigate the actions of trans-resveratrol on voltage-gated K(+) channels, which have been implicated in neuronal apoptosis. Superfusion of trans-resveratrol reversibly inhibited both the delayed rectifier (I(K)) and fast transient K(+) current (I(A)) in rat dissociated hippocampal neurons with IC(50) values of 13.6 +/- 1.0 microM and 45.7 +/- 7.5 microM, respectively. The inhibition on I(K) had a slow onset, was neither voltage dependent nor use dependent. Trans-resveratrol (30 microM) shifted the steady-state inactivation curve of I(K) to the hyperpolarizing direction by 20 mV and slowed down its recovery from inactivation. The inhibition on I(A) was similar to that on I(K), but voltage dependent. Superfusion of trans-resveratrol (30 microM) shifted the steady-state activation curve of I(A) to the depolarizing direction by 17 mV. Intracellular application of trans-resveratrol (30 microM) was ineffective. Based on the comparable effective concentrations, the inhibition of voltage-activated K(+) currents by trans-resveratrol may contribute to its neuroprotective effects.

Animals↗