To demonstrate the anti-inflammatory activity of Aronia melanocarpa fruit extract, human bronchial epithelial cells (BEAS-2B) were treated with lipopolysaccharide (LPS) and the effects of aronia bioactive fraction (ABF^®), anthocyanin enriched extract from the fruit of A. melanocarpa, were evaluated. Following pretreatment with ABF^® at 10–25 µg /mL, BEAS-2B cells were exposed to LPS and the expression of inflammatory mediators (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-8, regulated upon activation, normal T cell expressed and presumably secreted [RANTES], IL-1β, cyclooxygenase-2 [COX-2], and inducible nitric oxide synthase [iNOS]) was analyzed. In LPS-stimulated BEAS-2B cells, ABF^® pretreatment significantly decreased the mRNA expression of TNF-α, IL-6, IL-8, RANTES, IL-1β, and COX-2 at doses of 10 and 25 µg/mL. ABF^® also attenuated the secretion of TNF- α, IL-6, IL-8, and RANTES protein, as demonstrated by enzyme linked immunosorbent assay. Western blot analyses revealed the decreased expression of COX-2 and iNOS following ABF^® treatment. ROS production was decreased, and the cell cycle was arrested at the G0/G1 and S phases following ABF^® pretreatment. Our results suggest that ABF^® may have potential as a nutraceutical agent for the suppression of airway inflammation.

Obesity is caused by excessive fat cells and the overgrowth of adipocytes and is a major risk factor for several chronic illnesses. Aronia melanocarpa fruit is rich in anthocyanins and polyphenols and has protective effects against various diseases. In this study, we examined the effect of Aronia extract (Aronia bioactive fraction, ABF^®) on the biomarkers of the adipogenic pathway during adipocyte differentiation of 3T3-L1 cells. Lipid accumulation was verified by Oil Red O staining. mRNA and protein expression of lipoprotein lipase (LPL), CCAAT/enhancer-binding protein α (C/EBPα), peroxisome proliferator-activated receptor γ (PPARγ), fatty acid-binding protein 2 (FABP2), and fatty acid synthase (FAS) were assayed by RT-qPCR and Western blot analyses. Adiponectin and leptin secretion were measured using enzyme-linked immunosorbent assays. ABF^® treatment downregulated lipid accumulation based on Oil Red O staining. ABF^®-treated cells exhibited decreased mRNA and protein expression of LPL, C/EBPα, PPARγ, FABP2, and FAS. Moreover, ABF^® treatment significantly increased adiponectin secretion and decreased leptin secretion. In conclusion, ABF^® has anti-adipogenic effects on the differentiation of 3T3-L1 cells and may be used as an anti-obesity nutraceutical.

Preventing or reversing Tau hyperphosphorylation and aggregation represent critical objectives in the development of effective therapies for Alzheimer’s disease. The present study investigated the potential of a novel Aronia bioactive fraction—alginic acid nanocomplex (AANCP)—to simultaneously inhibit pathological features of Alzheimer’s disease. Evaluations of Aronia bioactive fraction (ABF) and low-molecular-weight alginic acid (LAA), utilized both individually and as AANCP, were conducted in HEK293-TauP301L and SH-SY5Y-TauP301L cell models of Alzheimer’s disease. Both ABF and LAA reduced the expression of total Tau and Tau phosphorylated at Ser396 in a concentration-dependent manner, with AANCP demonstrating significant synergistic activity of its components. Notably, the optimal AANCP ratio was 1:1 and 1:8 for inhibiting Tau phosphorylation and Tau aggregation, respectively. Mechanistically, AANCP inhibited Tau phosphorylation by upregulating p-Akt (phosphorylated protein kinase B) and p-GSK-3β (phosphorylated glycogen synthase kinase-3 beta), while also enhancing the activity of methylated PP2A, a key Tau phosphatase. Furthermore, AANCP exhibited superior efficacy in inhibiting heparin-induced Tau aggregation compared to the individual components. Analysis of autophagy markers indicated that the nanocomplex enhanced Tau clearance, as shown by increased LC3-II and Beclin-1 levels and reduced p62 levels. These results suggest AANCP as a promising therapeutic candidate that simultaneously reduces Tau phosphorylation and aggregation and facilitates autophagic Tau clearance, offering a potent, synergistic strategy for treating Alzheimer’s disease.