Açaí (Euterpe oleracea Mart) seed extract protects against maternal vascular dysfunction, hypertension, and fetal growth restriction in experimental preeclampsia

Objective To investigate whether Euterpe oleracea Mart. (açaí) seed extract (ASE) prevents maternal cardiovascular changes and intrauterine growth restriction (IUGR) in experimental preeclampsia (PE). Methods ASE administration (200 mg/kg/day) during mid to late pregnancy in a rat model of L-NAME-induced PE. Results ASE impaired the maternal hypertension and microalbuminuria as well as the lower fetal and placental weight in experimental PE. ASE also prevented the maternal vascular dysfunction and lipoperoxidation in this model. Conclusion ASE protected against maternal cardiovascular changes and IUGR in the L-NAME-induced PE. The protective effect of ASE may be partly explained by its antioxidant property

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Anxiolytic and antioxidant effects of Euterpe oleracea Mart. (açaí) seed extract in adult rat offspring submitted to periodic maternal separation

Many studies suggest a protective role of phenolic compounds in mood disorders. We aimed to assess the effect of Euterpe oleracea (açaí) seed extract (ASE) on anxiety induced by periodic maternal separation (PMS) in adult male rats. Animals were divided into 6 groups: control, ASE, fluoxetine (FLU), PMS, PMS+ASE, and PMS+FLU. For PMS, pups were separated daily from the dam for 3 h between postnatal day (PN) 2 and PN21. ASE (200 mg·kg−1·day−1) and FLU (10 mg·kg−1·day−1) were administered by gavage for 34 days after stress induction, starting at PN76. At PN106 and PN108, the rats were submitted to open field (OF) and forced swim tests, respectively. At PN110, the rats were sacrificed by decapitation. ASE increased time spent in the center area in the OF test, glucocorticoid receptors in the hypothalamus, tropomyosin receptor kinase B (TRKB) levels in the hippocampus, and nitrite levels and antioxidant activity in the brain stem (PMS+ASE group compared with PMS group). ASE also reduced plasma corticotropin-releasing hormone levels, adrenal norepinephrine levels, and oxidative damage in the brain stem in adult male offspring submitted to PMS. In conclusion, ASE treatment has an anti-anxiety effect in rats submitted to PMS by reducing hypothalamic–pituitary–adrenal axis reactivity and increasing the nitric oxide (NO)–brain-derived neurotrophic factor (BDNF)–TRKB pathway and antioxidant defense in the central nervous system. Novelty •ASE has anti-anxiety and antioxidant effects in early-life stress. •ASE reduces hypothalamic–pituitary–adrenal axis reactivity. •The anxiolytic effect of ASE may involve activation of the NO–BDNF–TRKB pathway in the central nervous system.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Mesenteric vascular reactivity.

<p>Effect of treatment with ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on vasodilator effects of ACh (A) and NG (B), and vasoconstrictor effects of NE (C) in mesenteric arterial bed from type 2 diabetic rats. Data are mean ± SEM, n = 10 for all groups. *Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Controls; ⁺Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Sedentary D.</p

Expression of insulin cascade and pAMPK protein.

<p>Effect of treatment with ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on IR (A), AKT (B), pAKT (C), GLUT-4 (D) and pAMPK expressions in skeletal muscle from type 2 diabetic rats. Data are mean ± SEM, n = 4 for all groups. Using one-way ANOVA: *Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Controls; ^●Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Training C; ⁺Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Sedentary D; ^$Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Training D; ^δSignificantly different (<i>p ≤ 0</i>.<i>05</i>) from ASE Sedentary D. Using unpaired Student's t-test: ^&Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Sedentary D.</p

Effects of ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on glucagon-like peptide-1 (GLP-1), leptin, and anti-inflammatory cytokine serum levels in type 2 diabetic animals.

<p>Effects of ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on glucagon-like peptide-1 (GLP-1), leptin, and anti-inflammatory cytokine serum levels in type 2 diabetic animals.</p

Glycemic levels and body weight.

<p>Effect of treatment with ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on blood glucose levels (A) and body weight (B) in type 2 diabetic rats. Data are mean ± SEM, n = 10 for all groups. *Significantly different (p<0.05) from Controls; ⁺Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Sedentary D; ^$Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Training D; ^δSignificantly different (<i>p ≤ 0</i>.<i>05</i>) from ASE Sedentary D.</p

Insulin resistance and β-cell function.

<p>Effect of treatment with ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on serum insulin levels (A), HOMA-IR (B) and HOMA-B (C) indexes in type 2 diabetic rats. Data are mean ± SEM, n = 6 for all groups. *Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Controls; ⁺Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Sedentary D. ^$Significantly different (<i>p ≤ 0</i>.<i>05</i>) from Training D.</p

Effects of ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on HbA1c serum levels and lipid profile in type 2 diabetic animals.

<p>Effects of ASE (200mg/Kg/day) and exercise training (30 min/day; 5 days per week) on HbA1c serum levels and lipid profile in type 2 diabetic animals.</p