Dong Keun Song

Inhibition of stress-induced plasma corticosterone levels by ginsenosides in mice: involvement of nitric oxide

GINSENG total saponins (GTS) injected intracere-broventricularly (i.c.v.) at doses of 0.1–1 μg inhibited the i.c.v. injection stress-induced plasma corticosterone levels in mice. The inhibitory action of GTS was blocked by co-administered NG-nitro-L-arginine methyl ester (L-NAME; 1.5 μg, i.c.v.), an inhibitor of nitric oxide synthase (NOS). Of the ginsenosides Rb1, Rb2, Rc, Rd, Re, Rf, Rg1, 20(S)-Rg3 and 20(R)-Rg3 injected i.c.v. at doses of 0.01–1 μg, 20(S)-Rg3 and Rc significantly inhibited the i.c.v. injection stress-induced plasma corticosterone levels. The inhibitory actions of 20(S)-Rg3 and Rc were blocked by co-administered L-NAME (1.5 μg, i.c.v.). These results suggest that GTS, 20(S)-Rg3 and Rc may inhibit the i.c.v. injection stress-induced hypothalamo-pituitary-adrenal response by inducing NO production in the brain.

Postischemic hypothermia induced by eugenol protects hippocampal neurons from global ischemia in gerbils

We studied whether eugenol provides neuroprotection against delayed neuronal death in the hippocampal CA1 region following a 5 min occlusion of the common carotid arteries bilaterally under either free-regulating temperature (TF) or maintained temperature (TM, 37 degrees C) conditions in gerbils. Right after occlusion of the carotid arteries, we injected eugenol intraperitoneally at concentrations of either 50, 100, or 200 mg/kg. There was significant preservation of neuronal cells in the CA1 region in the eugenol-treated groups 7 days after the ischemic insult in the TF condition, with respective survival values of 26, 43, and 68%. In the TM condition, however, significant neuroprotection was only seen with eugenol concentrations of 100 and 200 mg/kg (32% and 52%, respectively). When the rectal temperature was maintained at 38 degrees C for 30 min after occlusion of the carotid arteries, no reduction in CA1 damage was observed with any dose of eugenol. These results suggest that eugenol may provide neuroprotection against ischemic damage by its hypothermic action.

Effects of spinally and supraspinally injected 3-isobutyl1-methylxanthine, cholera toxin, and pertussis toxin on cold water swimming stress-induced antinociception in the mouse

1. The cold (4 degrees C) water swimming stress (CWSS) for 3 min significantly increased the inhibition of the tail-flick response in ICR mice. 2. Pertussis toxin (PTX, 0.05-0.5 microgram) in mice pretreated intrathecally (IT) for 6 days attenuated the inhibition of the tail-flick response induced by CWSS. However, intracerebroventricular (ICV) pretreatment with PTX at the same doses did not affect CWSS-induced inhibition of the tail-flick inhibition. 3. 3-Isobutyl-1-methylxanthine (IBMX, 0.01-1 ng) in mice pretreated IT for 10 min dose-dependently attenuated the inhibition of the tail-flick response induced by CWSS. However, IBMX in mice ICV pretreated ICV at the same doses was not effective in attenuating the CWSS-induced inhibition of the tail-flick response. 4. Neither IT nor ICV pretreatment with cholera toxin (CTX, 0.05-0.5 microgram) for 24 hr affected the inhibition of the tail-flick response induced by CWSS. 5. The ICV or IT injection of PTX, CTX, or IBMX did not affect the basal tail-flick response latency. 6. It is concluded that spinal, but not supraspinal, PTX-sensitive G-proteins and cAMP phosphodiesterase may be involved in the antinociception produced by CWSS. However, neither spinal nor supraspinal CTX-sensitive G-proteins appear to be involved in mediating the antinociception induced by CWSS.