Antioxidant-mediated protective role of Hericium erinaceus (Bull.: Fr.) Pers. against oxidative damage in fibroblasts from Friedreich’s ataxia patient

• Autor(a) principal: LEW,Sze-Yuen
• Data de Publicação: 2020
• Outros Autores: YOW,Yoon-Yen, LIM,Lee-Wei, WONG,Kah-Hui
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612020000500264
• topic: Hericium erinaceus; Friedreich’s ataxia; dermal fibroblasts; antioxidant; oxidative damage

Abstract Friedreich’s ataxia (FRDA) is a progressive neuromuscular disorder caused by substantial decrease of mitochondrial protein frataxin responsible for biogenesis of iron-sulphur clusters and protection from oxidative damage. In this study, we investigated the antioxidant activities of a standardized aqueous extract from fruiting bodies of Hericium erinaceus mushroom (HESAE) and its protective effects against oxidative damage induced by L-Buthionine sulfoximine (BSO) in fibroblasts derived from FRDA patient. The lactate dehydrogenase-based viability assay showed that FRDA fibroblast was sensitive to 12.5 mM BSO with a reduction of viability to 52.51 ± 13.92% after 24 h of BSO exposure. Interestingly, co-incubation with 32 mg/mL HESAE increased the viability to 85.35 ± 3.4%. Further, 12.5 mM BSO caused a decrease in the ratio of cellular reduced glutathione (GSH) to oxidised GSH (GSSG) that leads to cell death. Nevertheless, the damage was reduced by co-incubation with 32 mg/mL HESAE. Nuclear fluorescence staining revealed that 12.5 mM BSO induced cell death and the apoptosis was decreased by co-incubation with HESAE. These findings suggest the ability of HESAE in attenuating BSO-mediated cytotoxicity through maintenance of membrane integrity and optimal GSH/GSSG ratio, that are closely linked to its antioxidant activities. Further in vivo trials are highly warranted to clarify its potential benefits in management of FRDA.