Open AccessNeuroprotective effects of Fomes officinalis Ames polysaccharides on Aβ25–35-induced cytotoxicity in PC12 cells through suppression of mitochondria-mediated apoptotic pathway
Author(s) -
Ayijiang Habaike,
Mirensha Yakufu,
Cong Yao,
Yimin Gahafu,
Zhen Li,
Palida Abulizi
Publication year - 2020
Publication title -
cytotechnology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.488
H-Index - 62
eISSN - 1573-0778
pISSN - 0920-9069
DOI - 10.1007/s10616-020-00400-z
Subject(s) - cytochrome c , reactive oxygen species , mitochondrion , apoptosis , lactate dehydrogenase , superoxide dismutase , pharmacology , cytotoxicity , biochemistry , chemistry , malondialdehyde , oxidative stress , biology , microbiology and biotechnology , in vitro , enzyme
Aggregation of Aβ is a pathological hallmark of Alzheimer's disease (AD). The purpose of this study was to identify the protective roles of different polysaccharide components in Fomes officinalis Ames polysaccharides (FOAPs) against Aβ 25-35 -induced neurotoxicity in PC12 cells. Different doses of FOAPs components (i.e. FOAPs-a and FOAPs-b) were added to PC12 cells about 2 h before β-amyloid protein fragment 25-35 (Aβ 25-35 ) exposure. The AD cellular model of PC12 cells was established using Aβ 25-35 . Then the PC12 cells were divided into 9 groups including: control group, Donepezil hydrochloride (DHCL) group, model group treated using 40 μM Aβ 25-35 , followed by FOAPs-a and FOAPs-b interference (50, 100 and 200 μg/mL). The mitochondrial reactive oxygen species (ROS), ATP, superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH) and mitochondrial membrane potential (MMP) were determined by commercial kits. The Cytochrome C, Bcl-2 and Bax expressions in the mitochondria and cytosol was determined by using Western blot analysis. FOAPs-a and FOAPs-b could significantly inhibit the LDH release, MDA level and the over accumulation of ROS induced by Aβ 25-35 in PC12 cells in a dose-dependent manner. They could also effectively prevent Aβ 25-35 -stimulated cytotoxicity, which involved in attenuating cell apoptosis, increasing the ratio of Bcl-2/Bax and inhibiting Cytochrome C release from mitochondria to cytosol in PC12 cells. Moreover, FOAPs-a and FOAPs-b significantly alleviated mitochondrial dysfunction by regulating the MMP, as well as promoting the mitochondrial ATP synthesis. FOAPs-a and FOAPs-b played neuroprotective roles against Aβ 25-35 -induced cytotoxicity in PC12 cells through suppressing the mitochondria-mediated apoptotic pathway.