Antidepressant and Antiaging Effects of Açaí (Euterpe oleracea Mart.) in Mice.
José Rogério Souza-MonteiroGabriela P F ArrifanoAna Isabelle D G QueirozBruna S F MelloCharllyany S CustódioDanielle S MacêdoMoisés HamoyRicardo S O ParaenseLeonardo Oliveira BittencourtRafael Rodrigues LimaRommel R BurbanoHervé RogezCristiane do Socorro Ferraz MaiaBarbarella M MacchiJosé Luiz Martins do NascimentoMaria Elena Crespo-LópezPublished in: Oxidative medicine and cellular longevity (2019)
Depression is a mental disorder that affects 300 million people of all ages worldwide, but fewer than half of those with the condition receive adequate treatment. In addition, the high pharmacological refractoriness (affecting 30%-50% of patients) and toxicity of some classical antidepressants support the pursuit of new therapies. People with this condition show depressed mood, loss of pleasure, high levels of oxidative stress, and accelerated biological aging (decreased telomere length and expression of the telomerase reverse transcriptase (TERT), the enzyme responsible for telomere maintenance). Because of the close relationship between depression and oxidative stress, nutraceuticals with antioxidant properties are excellent candidates for therapy. This study represents the first investigation of the possible antidepressant and antiaging effects of commercial samples of clarified açaí (Euterpe oleracea) juice (EO). This fruit is rich in antioxidants and widely consumed. In this study, mice were treated with saline or EO (10 μL/g, oral) for 4 days and then with saline or lipopolysaccharide (0.5 mg/kg, i.p.) to induce depressive-like behavior. Only four doses of EO were enough to abolish the despair-like and anhedonia behaviors and alterations observed in electromyographic measurements. The antidepression effect of EO was similar to that of imipramine and associated with antioxidant and antiaging effects (preventing lipid peroxidation and increasing TERT mRNA expression, respectively) in three major brain regions involved in depression (hippocampus, striatum, and prefrontal cortex). Additionally, EO significantly protected hippocampal cells, preventing neuronal loss associated with the depressive-like state and nitrite level increases (an indirect marker of nitric oxide production). Moreover, EO alone significantly increased TERT mRNA expression, revealing for the first time a potent antiaging action in the brain that suggests neuroprotection against long-term age-related consequences.
Keyphrases
- oxidative stress
- prefrontal cortex
- nitric oxide
- cerebral ischemia
- induced apoptosis
- major depressive disorder
- bipolar disorder
- sleep quality
- depressive symptoms
- poor prognosis
- dna damage
- mental health
- newly diagnosed
- ischemia reperfusion injury
- ejection fraction
- white matter
- inflammatory response
- metabolic syndrome
- prognostic factors
- subarachnoid hemorrhage
- hydrogen peroxide
- toll like receptor
- diabetic rats
- signaling pathway
- multiple sclerosis
- stress induced
- stem cells
- type diabetes
- high fat diet induced
- long non coding rna
- adipose tissue
- immune response
- endoplasmic reticulum stress
- oxide nanoparticles
- cognitive impairment