Leaf mineral composition reflects the complex interaction between soil, climate, and plant genetic and epigenetic background in terms of organic and inorganic composition. The present study aimed to evaluate the effect of seven soil compositions on the mineral contents of Strawberry leaves (Arbutus unedo) under Moroccan conditions. The obtained results demonstrated a significant positive correlation between the soil nitrogen, phosphorus, and potassium levels and their levels in the Strawberry plant leaves. Also, a positive relation was reported between the soil organic matter and the level of manganese and phosphorus in leaves. Moreover, a significant negative correlation was demonstrated between the soil organic matter and the plant pH level. These correlations were confirmed by the principal component analysis (PCA) which demonstrated the presence of three principal components accounting for 54.42% of the total variations, reflecting the important proportions of the various patterns of mineral and organic traits among accessions. In PCA, the most discriminative traits were clustered in PC1 and PC2. These findings may highlight the specific mineral needs for the A. unedo plant for its optimal cultivation and subsequent domestication in Morocco.

Activation of the apoptotic pathway has been associated with promoting neuronal cell death in the pathophysiology of Parkinson disease (PD). Nonetheless, the mechanisms by which it may occurs remain unclear. It has been suggested that stress-induced oxidation and potentially apoptosis may play a major role in the progression of PD. Thus, in this study, we aimed to investigate the effect of subchronic restraint stress on striatal dopaminergic activity, iron, p53, caspase-3, and plasmatic acetylcholinesterase (AChE) levels in an animal model of PD induced by administration of 6-hydroxydopamine(6-OHDA) in the medial forebrain bundle (MFB). The obtained results showed that restraint stress exacerbates motor coordination deficits and anxiety in animals treated with 6-OHDA in comparison to animals receiving saline, and it had no effect on object recognition memory. On another hand, 6-OHDA decreased dopamine(DA) levels, increased iron accumulation, and induced overexpression of the pro-apoptotic factors caspase-3, p53, and AChE. More interestingly, post-lesion restraint stress exacerbated the expression of caspase-3 and AChE without affecting p53 expression. These findings suggest that subchronic stress may accentuate apoptosis and may contribute to DA neuronal loss in the striatal regions and possibly exacerbate the progression of PD.

Cerebral metabolic abnormalities are common in neurodegenerative diseases. Previous studies have shown that mitochondrial damage alters ATP production and increases Reactive Oxygen Species (ROS) release which may contribute to neurodegeneration. In the present study, we investigated the neuroprotective effects of cannabidiol (CBD), a non-psychoactive component derived from marijuana (Cannabis sativa L.), on astrocytic bioenergetic balance; in a primary cell culture model of lipopolysaccharide (LPS)-induced neurotoxicity. Astrocytic metabolic profiling using an extracellular flux analyzer demonstrated that CBD decreases mitochondrial proton leak, increased spare respiratory capacity and coupling efficiency in LPS-stimulated astrocytes. Simultaneously CBD increased astrocytic glycolytic capacity and glycolysis reserve in a cannabinoid receptor type 1 (CB1) dependent manner. CBD-restored metabolic changes were correlated with a significant decrease in the pro-inflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) concentration, and a reduction of ROS production in LPS-stimulated astrocytes. These results suggest that CBD may inhibit LPS-induced metabolic impairments and inflammation by enhancing astrocytic metabolic glycolysis versus oxidative phosphorylation through its action on CB1 receptors. The present findings suggest CBD as a potential anti-inflammatory treatment in metabolic pathologies and highlight a possible role for the cannabinoidergic system in the modulation of mitochondrial oxidative stress.

Chronic exposure to cocaine alters inflammatory signalling pathways in the brain, activates microglia and induces cognitive and motivational behavioural impairments. The endocannabinoid system may mediate cocaine’s effects. In the present study, we investigated the modulatory effects of the cannabinoid CB2 receptor agonist JWH-133 on cocaine-induced inflammation and motivational behavioural changes in vivo, and the possible effects of fractalkine (CX3CL1) on primary microglia metabolic activity and its subsequent contribution to cocaine-induced neurotoxicity. Our findings show that the CB2-specific receptor agonist, JWH-133, significantly attenuated the reinstatement of cocaine-induced CPP, increased Δ-FOSB expression in the nucleus accumbens (Nac), increased CX3CL1 levels in the ventral tegmental area (VTA) and prefrontal cortex (PFC), and decreased IL-1β in the PFC and NAc of cocaine treated animals. On the other hand, stimulation of the cortical primary microglial cells with CX3CL1 induced a biphasic effect. At a low concentration of 50 nM, CX3CL1 decreased mitochondrial oxidative metabolism vs glycolysis, and decreased the release of the proinflammatory cytokine, IL-1β, but did not affect TNFα. However, a dose of 100 nM of CX3CL1 increased mitochondrial oxidative metabolism, and both, IL-1β and TNFα release. These findings demonstrate that CB2 cannabinoid receptor modulation alters cocaine-induced reward-seeking behaviour and related neurobiological changes and highlights a potential role for CX3CL1 in the modulation of microglial metabolic and inflammatory-mediated activities.

Activation of the apoptotic pathway has been associated with promoting neuronal cell death in the pathophysiology of Parkinson disease (PD). Nonetheless, the mechanisms by which it may occurs remain unclear. It has been suggested that stress-induced oxidation and potentially apoptosis may play a major role in the progression of PD. Thus, in this study, we aimed to investigate the effect of subchronic restraint stress on striatal dopaminergic activity, iron, p53, caspase-3, and plasmatic acetylcholinesterase (AChE) levels in an animal model of PD induced by administration of 6-hydroxydopamine(6-OHDA) in the medial forebrain bundle (MFB). The obtained results showed that restraint stress exacerbates motor coordination de cits and anxiety in animals treated with 6-OHDA in comparison to animals receiving saline, and it had no effect on object recognition memory.On another hand, 6-OHDA decreased dopamine(DA) levels, increased iron accumulation, and induced overexpression of the pro-apoptotic factors caspase-3, p53, and AChE. More interestingly, post-lesion restraint stress exacerbated the expression of caspase-3 and AChE without affecting p53 expression.These ndings suggest that subchronic stress may accentuate apoptosis and may contribute to DA neuronal loss in the striatal regions and possibly exacerbate the progression of PD.