RESUMEN
Corticosteroids are widely used in medicine, for their anti-inflammatory and immunosuppressive actions, but can lead to troubling psychiatric side-effects. In fact, corticosteroids can induce many symptoms and syndromes, for example, mood disorders, anxiety and panic disorder, suicidal thinking and behavior. Furthermore, chronic stress and the administration of exogenous glucocorticoids are reported to induce affective changes in humans and rodents that relate to depressive state. Animal models are highly useful tools for studying the depression etiology. Face validity, construct validity, and predictive validity are the main criteria to evaluate animal depression models. The present study aimed to investigate the behavioral, cognitive, and biochemical effects of a chronic administration of DEX on Wistar rats. Wistar rats were administered daily with DEX (1.5 mg/kg, i.p., 21 days) or saline, the clomipramine treatment (2 mg/kg, i.p.) was realized just after the DEX injections for 21 days. DEX induced changes were evaluated by: forced swimming, novelty suppressed feeding, saccharin preference, open field, Morris water maze, and oxidative stress state in the brain. Results showed that chronic DEX administration conduct to a range of depression-related behavioral traits, including anhedonia, despair, weight loss, anxiety-like behavior, and cognitive impairments, which fill the face validity criterion. The DEX induced behavioral changes may result from the massive production of oxidative stress agents. This sustains the etiological hypothesis claiming that hyper-circulating glucocorticoid resulting from HPA dysfunction induces damage in certain neural structures related to depressive disorder, essentially the hippocampus. The antidepressant treatment has restored the behavioral state of rats which fills the predictive validity criterion.
RESUMEN
The present study investigates the potential neuroprotective effect of argan oil (AO), a natural vegetable oil, commonly used in folk Moroccan medicines, on adolescent intermittent ethanol intoxication (IEI), induced voluntary ethanol consumption, and withdrawal syndrome in rats. Animals were treated with ethanol (intraperitoneally [i.p.], 3 g/kg body weight [bw]) in intermittent doses (2 days on; 2 days off, from postnatal day 30-43), with/without oral AO pre-treatment (10 mL/kg/day bw, from postnatal day 21-121). A 2-bottle free access test was performed over 10 weeks to assess 10% ethanol consumption. Behavioral signs of withdrawal were observed after 2, 6, 24, 48, and 72 h after ethanol removal. Anxiety-like behaviors in the elevated plus maze and the light/dark box tests were also evaluated at 72 h of withdrawal. We found that AO pre-treatment significantly decreased the voluntary ethanol consumption induced by adolescent IEI. In addition, by establishing low ethanol consumption, AO pre-treatment counteracts negative effects of ethanol withdrawal and anxiety-like behaviors in ethanol-treated rats after 72 h of abstinence. Following behavioral assays, oxidative stress markers were evaluated and histologic analysis of neurodegeneration was also performed. The results showed that the low ethanol drinking in the AO-supplemented rats was associated with inhibition of oxidative stress and neurodegeneration in the rats' brains. These findings provide evidence for the promising neuroprotective effect of AO supplementation in voluntary ethanol consumption and withdrawal syndrome, at least in part through counteracting oxidative stress markers and neurodegeneration.