ArticleScientific reports2022
Polyphenol-rich açaí seed extract exhibits reno-protective and anti-fibrotic activities in renal tubular cells and mice with kidney failure.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Evaluating the Clinical Impact of a Polyphenol-Rich Extract fromNutrients · 2024Trial
- Biological Safety and Functional Properties of Açaí Seed Extract: Antioxidant Capacity and Prebiotic Potential.Journal of food science · 2026Article
- Açaí Seeds for a Greener Future: Transforming Agro-Waste into Industrial Value.Foods (Basel, Switzerland) · 2026Review
- Antioxidant, Anti-Inflammatory, and Antiapoptotic Effects ofPlants (Basel, Switzerland) · 2025Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main goal of this study was to evaluate the reno-protective effects of a phenolic-rich Açaí seed extract (ASE) in mice with kidney failure. Kidney failure was induced chemically with an adenine-rich diet (0.25% w/w for 4 weeks) in male CD1 Swiss mice. Mice were then provided daily with ASE (at a dose of ~ 350 mg/kg/day) in drinking water for 4 weeks. Adenine mice exhibited renal dysfunction evidenced by increased proteinuria, increased uremia, extensive tubular atrophy and kidney fibrosis associated with overexpression of pro-fibrotic genes (collagen 1a1, transforming growth factor β1, TGF-β1) and markers of tubular injury (such as Kidney injury molecule-1, KIM-1). ASE was able to beneficially counteract all these effects. ASE improved oxidative damage and fibrosis by decreasing carbonylated protein and MDA concentrations, as well as collagen deposition in renal tissue. ASE decreased the expression of TGF-β1 gene and the abundance of protein TGF-β1 in kidneys. It further decreased both expression and urinary excretion of tubular injury biomarkers, e.g., KIM-1 and Neutrophil gelatinase-associated lipocalin. CKD ASE-treated mice exhibited higher polyphenol content and total antioxidant capacity compared to control mice. ASE further prevented the expression of profibrotic genes in HK2 human tubular cells exposed to uremic toxins. Taken together, these findings suggest that ASE exerted potent reno-protective and anti-fibrotic effects through its antioxidant activity and the modulation of the TGF-β1 pathway.
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