scholarly journals Antiplatelet activity and chemical analysis of leaf and fruit extracts from Aristotelia chilensis

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250852
Author(s):  
Lyanne Rodríguez ◽  
Andrés Trostchansky ◽  
Irene Wood ◽  
Mauricio Mastrogiovanni ◽  
Hermine Vogel ◽  
...  

Aristotelia chilensis (Mol.) Stuntz, also known as maqui, is a plant native to Chile without chemical characterization and quantification of the bioactive compounds present in it. HPLC-UV and HPLC-MS/MS studies have shown the presence, at different concentrations, of phenolic and anthocyanin compounds in fruit and leave extracts of the domesticated maqui clones Luna Nueva, Morena, and Perla Negra. The extracts from leaves and unripe fruits of Luna Nueva and Morena clones significantly inhibit platelet aggregation induced by several agonists; the extracts inhibit platelet granule secretion by decreasing the exposure of P-selectin and CD63 at the platelet membrane. Reactive oxygen species formation in platelets is lower in the presence of maqui extracts. Statistical Pearson analysis supports the levels of phenolic and anthocyanin compounds being responsible for the antiaggregant maqui effects. This work is the first evidence of antiplatelet activity from Aristotelia chilensis giving added value to the use of leaves and unripe fruits from this species.

2018 ◽  
Author(s):  
Loïc Léger ◽  
Aurélie Budin-Verneuil ◽  
Margherita Cacaci ◽  
Abdellah Benachour ◽  
Axel Hartke ◽  
...  

2003 ◽  
Vol 17 (5-6) ◽  
pp. 803-810 ◽  
Author(s):  
Jalal Pourahmad ◽  
Peter J O‘Brien ◽  
Farzaneh Jokar ◽  
Bahram Daraei

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Daniel Edelmann ◽  
Bork A. Berghoff

Abstract Induction of growth stasis by bacterial toxins from chromosomal toxin-antitoxin systems is suspected to favor formation of multidrug-tolerant cells, named persisters. Recurrent infections are often attributed to resuscitation and regrowth of persisters upon termination of antibiotic therapy. Several lines of evidence point to oxidative stress as a crucial factor during the persister life cycle. Here, we demonstrate that the membrane-depolarizing type I toxins TisB, DinQ, and HokB have the potential to provoke reactive oxygen species formation in Escherichia coli. More detailed work with TisB revealed that mainly superoxide is formed, leading to activation of the SoxRS regulon. Deletion of the genes encoding the cytoplasmic superoxide dismutases SodA and SodB caused both a decline in TisB-dependent persisters and a delay in persister recovery upon termination of antibiotic treatment. We hypothesize that expression of depolarizing toxins during the persister formation process inflicts an oxidative challenge. The ability to counteract oxidative stress might determine whether cells will survive and how much time they need to recover from dormancy.


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