Acai (Euterpe oleracea Mart) modulates oxidative stress and inflammation by NF-κB inactivation and Nrf2 up-regulation in experimental diabetes
To evaluate the effects of acai extract (EA) on oxidative stress and inflammation induced by high glucose in cultured mouse immortalized mesangial cells (MiMC) and diabetic rats. MiMC cell viability and proliferation were determined by MTT. Extracellular and intracellular nitric oxide (NO) and intracellular ROS were also measured. The cell proteins were extracted for analysis of catalase, Nrf2, p-Nrf2, SOD-1, SOD-2, iNOS, NF-{kappa}B, p-NF-{kappa}B and TNF- expression. Male, adult Wistar rats were distributed into 3 groups: control (CTL) and diabetic (DM) rats who received water and DMEA and received 1 mL/day EA (200 mg/kg) via gavage for 8 consecutive weeks. After treatment with EA, metabolic profile, renal function and thiobarbituric acid reactives substances (TBARS) levels were evaluated, and kidneys were collected for qualitative histological analysis. EA maintained cell viability above 90% in all groups; it decreased proliferation in the HG group, both significant. NO levels, ROS generation, iNOS, NF-{kappa}B, p-NF-{kappa}B and TNF- expression were reduced significantly after 72 h of EA treatment, with significant increases for all antioxidants studied. DMEA vs DM showed a significant increase in body weight, improved kidney function and reduced TBARS excretion. EA treatment decreased proliferation, oxidative stress and inflammation in MiMC, and although acai did not decrease fasting glucose, it recovered the body weight and delayed the decline of renal function in the diabetic animals, suppressing the signaling of inflammatory mediators via NF-{kappa}B inactivation and increasing all antioxidants studied by upregulating the Nrf2 response pathway.