Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/114000
Title: Brassica oleracea Var italica by-Products Prevent Lipid Accumulation and Cell Death in a Liver Cell Model of Lipid Toxicity
Authors: Castelão-Baptista, José P. 
Valente, Sara A. 
Canário, Sara 
Oppolzer, David
Barros, Ana
Venâncio, Carlos
Martins, Tânia 
Antunes, Luís
Sardão, Vilma A. 
Rosa, Eduardo
Oliveira, Paulo J. 
Keywords: phytochemicals; NAFLD; HepG2; natural products; FFA
Issue Date: 12-Feb-2023
Publisher: MDPI
Project: PTDC/ASP-HOR/29152/2017 
UIDB/04033/2020 
UIDB/04539/2020 
info:eu-repo/grantAgreement/UIDP/04539/2020 
LA/P/0058/2020 
H2020-WIDESPREAD-2018-01 
Serial title, monograph or event: Nutrients
Volume: 15
Issue: 4
Abstract: Obesity, a rising concern in the Eastern world, encompasses several co-morbidities, namely non-alcoholic fatty liver disease (NAFLD). Potential natural-based interventions to decrease the burden of obesity complications are being investigated. Many of the edible parts of plants are not sold for consumption and end up as massive waste, losing nutritional potential. In fact, a sizeable amount of waste is generated within the different steps of the food supply chain, representing a massive loss of both plant material and natural resources. A good example is Brassica by-products (BBPs). The objective of this work was to investigate the effect of three different extracts from broccoli (Brassica oleracea var italica) by-products in an in vitro model of free fatty acid (FFA)-induced lipotoxicity using human hepatoma HepG2 cells. Broccoli leaf, stalk, and inflorescence extracts induced a dose-dependent decrease in the cell viability of HepG2 cells. However, the maximal non-lethal concentrations of leaves, stalks, and inflorescences (10 μg/mL) did not compromise mitochondrial function or neutral lipid accumulation in HepG2 cells. The extracts significantly decreased FFA-induced lipid accumulation in HepG2 cells either in a co-incubation or pre-incubation strategy. The broccoli extracts' capacity to prevent the FFA-induced decrease in catalase activity in HepG2 may explain the observed effects.
URI: https://hdl.handle.net/10316/114000
ISSN: 2072-6643
DOI: 10.3390/nu15040924
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais

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