Dietary administration of cumin-derived cuminaldehyde induce neuroprotective and learning and memory enhancement effects to aging mice.

Cuminaldehyde (CA) is one of the major compounds of the essential oil of Cuminum cyminum. The aim of this study was to evaluate the effects of CA on aging, specifically on spatial learning and memory. To achieve our objective, an in vitro study on SH-SY5Y cells was performed to analyze the neuroprotective effect of CA against dexamethasone using the MTT assay. An in vivo study was performed for evaluation of the spatial learning and memory using Morris water maze (MWM). RT-PCR was performed to quantify the expression of specific genes (Bdnf, Icam and ApoE) in the mice brain. The results obtained showed a neuroprotective effect of CA against dexamethasone-induced neuronal toxicity. The escape latency of CA-treated aged mice was significantly decreased as compared to the water-treated aged mice after 4 days of training in MWM. Moreover, CA treatment up-regulated the gene expression of Bdnf, Icam and ApoE, while it down-regulated the gene expression of IL-6. These findings suggest that CA has a neuroprotective effect, as well as a spatial learning and memory enhancement potential through the modulation of genes coding for neurotrophic factors and/or those implicated in the imbalance of neural circuitry and impairment of synaptic plasticity. Cuminaldehyde (CA) is one of the major compound of the essential oil of Cuminum cyminum. The aim of this study was to evaluate the effects of CA on aging, specifically on spatial learning and memory. To achieve our objective, an in vitro study on SH-SY5Y cells was performed to analyze the neuroprotective effect of CA against dexamethasone using the MTT assay. An in vivo study was performed for evaluation of the spatial learning and memory using Morris water maze (MWM). RT-PCR was performed to quantify the expression of specific genes (Bdnf, Icam and ApoE) in the mice brain. The results obtained showed a neuroprotective effect of CA against dexamethasone-induced neuronal toxicity. The escape latency of CA-treated aged mice was significantly decreased as compared to the water-treated aged mice after 4 days of training in MWM. Moreover, CA treatment up-regulated the gene expression of Bdnf, Icam and ApoE, while it down-regulated the gene expression of IL-6. These findings suggest that CA has a neuroprotective effect, as well as a spatial learning and memory enhancement potential through the modulation of genes coding for neurotrophic factors and/or those implicated in the imbalance of neural circuitry and impairment of synaptic plasticity.

Elucidation of the Molecular Mechanism Underlying Lippia citriodora(Lim.)-Induced Relaxation and Anti-Depression.

Lippia citriodora ethanolic extract (VEE) and verbascoside (Vs), a phenypropanoid glycoside, have been demonstrated to exert relaxant and anxiolytic properties. However, the molecular mechanisms behind their effects are still unclear. In this work, we studied the effects and action mechanisms of VEE and Vs in vivo and in vitro, on human neurotypic SH-SY5Y cells.TST was conducted on mice treated orally with VEE (25, 50 and 100 mg/Kg), Vs (2.5 and 5 mg/Kg), Bupropion (20 mg/Kg) and Milli-Q water. Higher dose of VEE-treated mice showed an increase of immobility time compared to control groups, indicating an induction of relaxation. This effect was found to be induced by regulation of genes playing key roles in calcium homeostasis (calcium channels), cyclic AMP (cAMP) production and energy metabolism. On the other hand, low doses of VEE and Vs showed an antidepressant-like effect and was confirmed by serotonin, noradrenalin, dopamine and BDNF expressions. Finally, VEE and Vsenhancedcell viability, mitochondrial activity and calcium uptake in vitro confirming in vivo findings. Our results showed induction of relaxation and antidepressant-like effects depending on the administered dose of VEE and Vs, through modulation of cAMP and calcium.