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Protective effects of a Ganoderma atrum polysaccharide against acrylamide induced oxidative damage via a mitochondria mediated intrinsic apoptotic pathway in IEC-6 cells.
Jiang, Guoyong; Zhang, Lulu; Wang, Hui; Chen, Qian; Wu, Xiaolin; Yan, Xiaoli; Chen, Yi; Xie, Mingyong.
Afiliação
  • Jiang G; State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, Peoplés Republic of China. chenyi15@ncu.edu.cn chenyi-417@163.com.
Food Funct ; 9(2): 1133-1143, 2018 Feb 21.
Article em En | MEDLINE | ID: mdl-29362765
ABSTRACT
The preventive role of a purified Ganoderma atrum polysaccharide PSG-1-F2 as a new dietary antioxidant against the intestinal toxicity of acrylamide (ACR) was investigated in vitro. Our results showed that ACR could induce oxidative stress in IEC-6 cells by the overproduction of reactive oxygen species (ROS) and malondialdehyde (MDA), and as well as the reduction in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In addition, the induction of a mitochondria-mediated intrinsic apoptotic pathway by ACR was evidenced by the events of loss of mitochondrial membrane potential, bax/bcl-2 dysregulation, cytochrome c release, and activation of caspase-3. Interestingly, PSG-1-F2 was able to suppress ACR toxicity by improving the redox status of IEC-6 cells and by attenuating mitochondria-mediated apoptosis. Its protective effect was even superior to the clinically used antioxidant N-acetylcysteine (NAC). This study uniquely introduces PSG-1-F2 as a potential inhibitor of ACR-induced stress and toxicities.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Polissacarídeos / Extratos Vegetais / Apoptose / Estresse Oxidativo / Acrilamida / Ganoderma / Mitocôndrias Idioma: En Revista: Food Funct Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Polissacarídeos / Extratos Vegetais / Apoptose / Estresse Oxidativo / Acrilamida / Ganoderma / Mitocôndrias Idioma: En Revista: Food Funct Ano de publicação: 2018 Tipo de documento: Article