Abstract
Agonists of CB1 and NMDA receptors decrease the toxic effect of organophosphorus compound paraoxon on PC12 cells
Highlights
[3,4,5,6]. It was shown that cannabinoid type 1 receptors (CB1) receptor expression is altered at variousneurodegenerative diseases [7,8,9,10,11]
We found that application of ACEA (CB1 receptor agonist), NMDA (NMDA receptor agonist) or both agonists increased cell survival vs the POX group (P < 0.001) indicating the neuroprotective effect against paraoxon
To determine whether the neuroprotective effect of ACEA was cannabinoid type 1 receptors (CB1) receptor-mediated, PC12 cells were treated with AM251 for 15 min prior to ACEA addition
Summary
[3,4,5,6]. It was shown that CB1 receptor expression is altered at variousneurodegenerative diseases [7,8,9,10,11]. We found that application of ACEA (CB1 receptor agonist), NMDA (NMDA receptor agonist) or both agonists increased cell survival vs the POX group (P < 0.001) indicating the neuroprotective effect against paraoxon. Incubation of PC12 cells with 100 μM POX for 48 h significantly decreased the level of GSH compared with control group (Fig. 2, p < 0.01).
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