ABSTRACT
Oncogene and antioncogene play contrary effects on the cell growth and proliferation controlling process, and cancer occurs when the presence of imbalance expression between them. That means there is yin-yang relationship between oncogene (yang) and antioncogene (yin), and also inside both of them. Taking the oncogene myc and antioncogene p53 for example, the yin gene p53 acts, in the yin side, to promote cell apoptosis and inhibit cell growth, while in the yang side, it facilitates for repairing the injured DNA to keep cell survival; the yang gene myc, promoting cell growth and proliferation in the yang side and inducing cell apoptosis in the yin side. To elucidate the yin-yang reactions between oncogene and antioncogene would be of important significance in the all-round and profound research of cancer.
Subject(s)
Humans , Genes, Tumor Suppressor , Medicine, Chinese Traditional , Neoplasms , Genetics , Oncogenes , Genetics , Proto-Oncogene Proteins c-myc , Metabolism , Tumor Suppressor Protein p53 , Metabolism , Yin-YangABSTRACT
<p><b>AIM</b>To test the antiepileptic effect of phencynonate hydrochloride and investigate its antiepileptic mechanism.</p><p><b>METHODS</b>Through establishment of different epilepsy models, antiepileptic effects of phencynonate hydrochloride and other drugs were examined. Besides, the effect of phencynonate hydrochloride and other compounds against NMDA-induced lethality in mice, NMDA-induced injury in rat primary hippocampal neuronal cultures and NMDA-induced current were also observed.</p><p><b>RESULTS</b>Phencynonate hydrochloride produced a significant anticonvulsant effect on different epilepsy models. Furthermore, phencynonate hydrochloride also exerted its obvious protection against the lethal effects of NMDA in mice, antagonized the NMDA-induced injury in rat primary hippocampal neuronal cultures and blocked NMDA-induced current in a dose-dependent manner.</p><p><b>CONCLUSION</b>Phencynonate hydrochloride had a notable anticonvulsant effect on typical epilepsy models, its antiepileptic mechanism might relate to its antagonism against NMDA receptor.</p>
Subject(s)
Animals , Female , Male , Mice , Rats , Animals, Newborn , Anticonvulsants , Pharmacology , Therapeutic Uses , Aza Compounds , Pharmacology , Therapeutic Uses , Cells, Cultured , Electroshock , Glycolates , Pharmacology , Therapeutic Uses , Hippocampus , Cell Biology , Lethal Dose 50 , N-Methylaspartate , Toxicity , Neurons , Neuroprotective Agents , Pharmacology , Pentylenetetrazole , Rats, Wistar , Seizures , Drug TherapyABSTRACT
To compare the difference in action sites between mecamylamine (MEC) and hexamethonium (HEX) on nicotinic receptors of sympathetic neurons, we investigated the effects of MEC and HEX on the nicotine-induced currents in cultured superior cervical ganglion neurons by whole-cell patch clamp technique. The IC(50) of MEC and HEX for antagonizing the effect of 0.08 mmol/L nicotine was 0.0012 and 0.0095 mmol/L, respectively. Both MEC and HEX accelerated the desensitization of nicotinic receptors. Furthermore, by comparing their effects at holding potentials 30, 70 and 110 mV, it was indicated that their suppressing effect on the nicotine-induced currents was voltage-dependent. However, different from that of HEX, the inhibitory effect of MEC increased with administering the mixture of MEC and nicotine at intervals of 3 min, indicating a use-dependent effect of MEC. It is concluded that the action site of MEC on nicotinic receptors of sympathetic neurons is different from that of HEX.
