Medicinal species as MTDLs: Turnera diffusa Willd. Ex Schult inhibits CNS enzymes and delays glutamate excitotoxicity in SH-SY5Y cells via oxidative damage

被引:26
作者
Bernardo, Joao [1 ]
Ferreres, Federico [2 ]
Gil-Izquierdo, Angel [2 ]
Valentao, Patricia [1 ]
Andrade, Paula B. [1 ]
机构
[1] Univ Porto, Fac Farm, Dept Quim, REQUIMTE,LAQV,Lab Farmacognosia, Rua Jorge Viterbo Ferreira 228, P-4050313 Oporto, Portugal
[2] CSIC, CEBAS, Dept Food Sci & Technol, Res Grp Qual Safety & Bioact Plant Foods, POB 164,Campus Univ Espinardo, Murcia 30100, Spain
关键词
Medicinal species; Turnera diffusa; Flavonoids; Neuroprotection; CNS enzymes; Glutamate excitotoxicity; HPLC-DAD-ESI/MSN; ALZHEIMERS-DISEASE; PHENOLIC-COMPOUNDS; INDUCED APOPTOSIS; FLAVONOIDS; ACETYLCHOLINESTERASE; LUTEOLIN; BUTYRYLCHOLINESTERASE; ANTIOXIDANT; BIOACTIVITY;
D O I
10.1016/j.fct.2017.06.014
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
One of the most promising approaches to confront the complexity of central nervous system disorders are new multi-target directed ligands (MTDLs). Five medicinal species (Cereus grandiflorus (L) Mill., Hyssopus officinalis L, Acorus calamus L, Silybum marianum L Gaertn. and Turnera diffusa Willd. Ex Schult), selected for their ethnopharmacological relevance, were object for in vitro screening. The aqueous extract of T. diffusa revealed the strongest neuroactivepotential, inhibiting monoamine oxidaseA (IC50 = 129.80 +/- 11.97 mu g/mL), and acetyl- and butyrylcholinesterase (IC25 = 0352 +/- 0.011 and 0.370 +/- 0.036 mg/mL, respectively). Its phenolic profile was established for the first time by HPLC-DADESI/MSn. Twenty-six out of thirty-seven compounds were hewly identified in this species. The pretreatment with this fiavonoid-rich extract promoted a rightward shift of the glutamate concentration neuronal cell (SH-SY5Y) death response curve. Furthermore, it significantly reduced the early phase formation of intracellular reactive species after glutamate and t-BHP exposure, suggesting that neuroprotection in SH-SY5Y cells was, in part, mediated by antioxidant mechanisms. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:466 / 476
页数:11
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