The 2011 edition of the Annual Meeting of the Brazilian Federation of Experimental Biology Societies (FeSBE, Federação de Sociedades de Biologia Experimental) took place from August 24th through 27th, in Rio de Janeiro, Brazil. Scientists from all over the world attended this meeting. We sent two brief communications in poster form.
Poster 1: EVALUATION OF THE ANALGESIC EFFECT OF VENLAFAXINE, A SEROTININ AND NORADRENALINE REUPTAKE INHIBITOR.
The aim of this study was to test the
analgesic effects of the antidepressant venlafaxine in several
experimental models of nociception.
Methods and Results:
Acetic
acid-induced writhing: Groups of six to twelve mice were administered
i.p. 0.6% acetic acid (10 mL kg−1, i.p.), and the number of abdominal
contractions was registered for 20 min, starting 30 min after the
injection. Animals were pre-treated with venlafaxine (10, 20, 40 and 60
mg kg−1, i.p.), 30 min before acetic acid administration. DMSO 5% was
used as vehicle (control group). With the exception of 10 mg kg−1, all
other doses of venlafaxine (20, 40 and 60 mg kg−1, i.p) produced
significant inhibition of writhing (p<0,05) (16.2±12.0, 11.6±8.0 and
3.7±2.0 respectively) when compared with control group (34.0±13.2).
Hot-plate test: groups of nine mice were treated with venlafaxine (10,
20, 40 and 60 mg kg−1, i.p.), 5% DMSO (controls) or morphine (10 mg
kg−1, i.p.) as standard. Measurements were performed before (time 0) and
after 30, 60 and 90 min from drug administration; a cut-off time of 45
seconds was used to avoid paw lesions. Only 60 mg/Kg, i.p. of
venlafaxine showed a significant effect on latency time to licking or
jumping (24.06±4.99 s) when compared with control group (6.88±1.15 s) on
time of 30 min. Morphine (10 mg kg−1, i.p. showed a significant effect
(p<0.05) (39.5±4.13, 34.5±5.54, 29.4±5.08 s) when compared to control
group (6.88±1.15, 6.58±1.88, 8.77±2.27 s) on times of 30, 60 and 90 min
respectively. Rota-rod test: Groups of six mice were treated with
venlafaxine (10, 20, 40 and 60 mg/kg, i.p.) and placed on the rota-rod
30 min after the injection. DMSO 5% was used as vehicle (control group).
The number of falls was recorded by one minute and the length of stay
in the bar. No difference between groups treated with venlafaxine and
control group was observed in any period of time. Statistical analysis:
All values were expressed as means±S.D.M. Data were analyzed using ANOVA
followed by Tukey test (p<0.05 was considered significant).
Conclusions:
These
results corroborate research that reported the inhibitory effect of
venlafaxine on the signs of spontaneous pain and hindpaw mechanical and
thermal hypersensitivity in animal models of tonic nociception and
neuropathic pain. Studies continue in an attempt to elucidate the action
mechanisms of these effects.
Link to this abstract: http://bit.ly/qrPHK7
Link to this poster in google docs: http://bit.ly/nJXtR5
Poster 2: EVALUATION OF ANTIPLATELET ACTIVITY OF MONOTERPENE PULEGONE
Objectives: To evaluate the antiplatelet activity of Pulegone in human PRP.
Methods and Results:
Platelet
aggregation was measured according to the method of Born and Cross (J
Physiol. 163; 178-195, 1963). Briefly, platelet aggregation was induced
at 37ºC in the aggregometer, with stirring at 1000 rpm, by addition of
ADP (4µM) as agonist. The resulting aggregation, measured as the change
in light transmission, was recorded for 5 min and presented as percent
aggregation related to control (100%). Pulegone oil (PUL) was emulsified
with Tween 80 (660 µg mL−1, control) and concentrations of 110, 220,
440 and 660 µg mL−1 were used. PUL 220, 440 and 660 µg mL−1 reduced
significantly (p<0.001) the platelet aggregation induced by ADP (4µM)
in 39.8, 47.3 and 70.1% (60.2±27.5; 52.7±17.23 and 29.9±7.60%
aggregation) respectively when compared to control group. Statistical analysis: All values are expressed as mean ±
SD. Differences between the sample-treated and control groups were
submitted to analysis of variance (ANOVA) followed by Tukey-Newman-Keuls
test for multiple comparisons (p< 0.05) was considered significant.
Conclusions:
Direct
stimulation of platelets by ADP results in shape change, reversible
aggregation at physiological concentrations of calcium, and finally,
desensitization. Transduction of the ADP signal involves a transient
rise in free cytoplasmic calcium, due to the mobilization of internal
stores and secondary store-mediated influx, and a concomitant inhibition
of adenylyl cyclase activity. It is possible that the antiplatelet
effect of pulegone is due to blocking of a step of ADP-induced platelet
stimulation.
Link to this abstract: http://bit.ly/pvZGwU
Link to this poster in google docs: http://bit.ly/nfyk3w
Link to FESBE 2011 program: http://bit.ly/ramXDw
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