RESUMO
Two models, mouse hot plate and vocalization indused by electrical stimulation of rat's tail were used to demonstrate the antinocice-ptive action of the neurotoxin ( NT ) from cobra venom.The paw-lick latencies of mice of both NT groups in different dose (0.023 mg/kg, 0.03 mg/kg, im ) were significantly prolonged than that of the control group. In the rats, the vocalization threshold of NT group was significantly higher than that of the control group too. This action of NT showed in these models was in good dose-resp-onse relationship. The onset of antinociceptive action of NT was 2 h and reached highe level 3h after intramuscular injection. This effect could be maintained for more than 24 h 3 groups of mice were continuously given normal saline, NT and morphine respectively for 9 days, and no tolerance showed in NT group of mice, but the acute tolerance to morphine occured in morphine group of mice. These result suggested that the analgesic mechanism of NT may be quite different from that fo morphine.
RESUMO
AIM: To explore the mechanism of nicotine against the apoptosis induced by colchicines in rat cortical neurons.METHODS: Cortical neurons were cultured from newborn Sprague-Dawley(SD) rats(less than 12 h).The rate of apoptosis was measured by Hoechst33258 fluorescence staining in the neurons,and the activity of Akt473 was analyzed by assay kit Akt473.RESULTS: The apoptosis of cortical neurons can be induced by 0.1 ?mol/L colchicine.The phosphorlation of Akt 473 decreased significantly(1/3 times of the control group,P