No abstract

ASE substantially reduced renal injury and prevented renal dysfunction by reducing inflammation, oxidative stress and improving the renal filtration barrier, providing a nutritional resource for prevention of diabetic and hypertensive-related nephropathy.

Açai fruit has been studied for its antioxidant properties, with positive feedback against many diseases, including cancer. Although açai seeds are not edible, their composition has been studied in order to find new applications and reduce garbage generation. This study aimed to evaluate the cytotoxic effects and impacts on the cell cycle and apoptosis of açai seed extract (ASE) on human lung carcinoma cell line (A549). Antioxidant activity of açai seed extract (ASE) was measured by DPPH assay, Trolox Equivalent Antioxidant Capacity (ABTS/TEAC), Ferric Reducing Ability (FRAP) and Oxygen radical absorbance capacity (ORAC) assays. Human lung carcinoma cell viability (A549) was monitored by MTT assay method and the effects on cell cycle and apoptosis were measured by flow cytometry. The results indicate high antioxidant activity in ASE and high values of total phenolic compounds (37.08 ± 8.56 g gallic acid/100 g). The MTT assay showed a maximum decrease (72.07%) in the viability of A549 cells after 48 h treatment with ASE (200 µg/mL). Flow cytometer analysis revealed that ASE increased the percentage of cells in G0/G1 phase and promoted a high increase of apoptotic cells when compared to the untreated cells. The present study suggests that ASE has a high antioxidant capacity and may have a protective effect against lung cancer.

To investigate the systemic and placental oxidant status as well as vascular function in experimental preeclampsia (PE) induced by nitro-L-arginine methyl ester (L-NAME). Fetal parameters and maternal blood pressure, proteinuria, mesenteric arterial bed (MAB) reactivity, and systemic and placental oxidative stress were compared between four groups: pregnant rats receiving L-NAME (60 mg/kg/day, orally) (P + L-NAME) or vehicle (P) from days 13 to 20 of pregnancy and nonpregnant rats receiving L-NAME (NP + L-NAME) or vehicle (NP) during 7 days. L-NAME administration during pregnancy induced some hallmarks of PE, such as hypertension and proteinuria. The P + L-NAME group presented lower weight gain and placental mass as well as reduced number and weight of live fetuses than P group. The vasodilator effect induced by acetylcholine (ACh) and angiotensin II (Ang II) was lower in the perfused MAB from NP + L-NAME and P + L-NAME than in control groups. Otherwise, the nitroglycerine-induced vasodilation and the phenylephrine- and Ang II-induced vasoconstriction were higher in MAB from NP + L-NAME and P + L-NAME groups than in the respective controls. Systemic and placental oxidative damage, assessed by malondialdehyde and carbonyl levels, was increased and activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were reduced in P + L-NAME and NP + L-NAME groups compared to controls. The present data suggest that the oxidative stress and reduced bioavailability of nitric oxide may contribute to attenuation of vasodilator responses to ACh and Ang II, and hyperreactivity to Ang II in the mesentery of preeclamptic rat, which may contribute to the increased peripheral vascular resistance and BP, as well as intrauterine growth restriction in L-NAME-induced PE.

No abstract

Objectives Obesity is considered a risk factor for the development of non-alcoholic fatty liver disease (NAFLD). The hydroalcoholic extract obtained from the ac ßai seed (ASE), rich in proanthocyanidins, has been shown a potential body weight regulator with antioxidant properties. This study aimed to investigate the therapeutic effect of ASE in obesity-associated NAFLD and compare it with Rosuvastatin. Methods Male C57BL/6 mice received a high-fat diet or standard diet for 12 weeks. The treatments with ASE (300 mg/kg per day) or rosuvastatin (20 mg/ kg per day) began in the eighth week until the 12th week. Key findings Our data show that the treatments with ASE and rosuvastatin reduced body weight and hyperglycaemia, improved lipid profile and attenuated hepatic steatosis in HFD mice. ASE and Rosuvastatin reduced HMGCoA-Reductase and SREBP-1C and increased ABGC8 and pAMPK expressions in the liver. Additionally, ASE, but not Rosuvastatin, reduced NPC1L1 and increased ABCG5 and PPAR-a expressions. ASE and rosuvastatin increased SIRT-1 expression and antioxidant defence, although only ASE was able to decrease the oxidative damage in hepatic tissue. Conclusions The therapeutic effect of ASE was similar to that of rosuvastatin in reducing dyslipidemia and hepatic steatosis but was better in reducing oxidative damage and hyperglycaemia.

Many evidences suggest a protective role of phenolic compounds on mood disorders. We aimed to assess the effect of the açaí seed extract (ASE) on anxiety induced by periodic maternal separation (PMS) in adult male rats. Animals were subdivided into six groups: Control, ASE, fluoxetine (FLU), PMS, PMS+ASE, and PMS+FLU. For PMS, pups were separated daily from the dam for 3hrs between postnatal day (PN)2–PN21. ASE (200mg/Kg/day) and FLU (10mg/Kg/day) were administered by gavage for 34 days after stress induction, starting at PN76. In PN106 and PN108, the rats were submitted to open field (OF) and forced swim tests, respectively. In PN110 the rats were sacrificed by decapitation. ASE increased the time spent in the center area in OF test, glucocorticoid receptors in the hypothalamus, TRKB receptors in the hippocampus, nitrite levels and antioxidant activity in brainstem from PMS+ASE group compared with the PMS group. ASE also reduced the corticotropin-releasing hormone plasma levels, norepinephrine adrenal levels, and oxidative damage in the brainstem from adult male offspring submitted to PMS. In conclusion, ASE treatment has an anti-anxiety effect in rats submitted to PMS by reducing hypothalamus-pituitary-adrenal axis reactivity and increasing NO-BDNF-TRKB pathway and antioxidant defense in the central nervous system. Novelty • Anti-anxiety and antioxidant effect of açaí in early life stress. • ASE reduces hypothalamus-pituitary-adrenal axis reactivity. • The anxiolytic effect of ASE may involve the activation of the NO-BDNF-TRKB pathway in the central nervous system.

The results suggest that the reduction of BP to normal values at the end of pregnancy in SHR may be related to an increased NO production and vasorelaxation to Ang II and Ang-(1-7) associated with decreased expression of vascular ACE and AT(1) receptors and oxidative status.