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Ginkgo biloba extract inhibits hippocampal neuronal injury caused by mitochondrial oxidative stress in a rat model of Alzheimer's disease.
Xia, Chenyi; Zhou, Mingmei; Dong, Xianwen; Zhao, Yan; Jiang, Meifang; Zhu, Guoqin; Zhang, Zhixiong.
Affiliation
  • Xia C; School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  • Zhou M; Institute of Interdisciplinary Integrative Medicine Research, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  • Dong X; Department of Children Rehabilitation Medicine, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
  • Zhao Y; School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
  • Jiang M; SPH XingLing Sci. & Tech. Pharmaceutical Co., Ltd., Shanghai, China.
  • Zhu G; SPH XingLing Sci. & Tech. Pharmaceutical Co., Ltd., Shanghai, China.
  • Zhang Z; School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
PLoS One ; 19(8): e0307735, 2024.
Article in En | MEDLINE | ID: mdl-39106233
ABSTRACT
Ginkgo biloba extracts (GBE) have been shown to effectively improve cognitive function in patients with Alzheimer's disease (AD). One potential therapeutic strategy for AD is to prevent loss of adult hippocampal neurons. While recent studies have reported that GBE protects against oxidative stress in neurons, the underlying mechanisms remain unclear. In this study, an AD-like rat model was established via bidirectional injection of amyloid beta 25-35 (Aß25-35; 20 µg) in the hippocampal CA1 region. Learning and memory abilities of experimental rats were AD assessed in response to oral administration of 7.5 g/L or 15 g/L Ginkgo biloba extract 50 (GBE50) solution and the peroxidation phenomenon of hippocampal mitochondria determined via analysis of mitochondrial H2O2 and several related enzymes. Levels of the oxidative stress-related signaling factor cytochrome C (Cyto C), apoptosis-related proteins (Bax, Bcl-2 and caspase-3) and caspase-activated DNase (CAD) were further detected via western blot. 8-Hydroxydeoxyguanosine (8-OHdG), the major product of DNA oxidative stress, was evaluated to analyze DNA status. Our results showed elevated H2O2 levels and monoamine oxidase (MAO) activity, and conversely, a decrease in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the hippocampus of AD rats. Administration of GBE50 regulated the activities of these three enzymes and induced a decrease in H2O2. GBE50 exerted regulatory effects on abnormally expressed apoptotic proteins in the AD rat hippocampus, enhancing the expression of Bcl-2, inhibiting release of Cyto C from mitochondria, and suppressing the level of caspase-3 (excluding cleaved caspase-3). Furthermore, GBE50 inhibited DNA damage by lowering the generation of 8-OHdG rather than influencing expression of CAD. The collective findings support a protective role of GBE50 in hippocampal neurons of AD-like animals against mitochondrial oxidative stress.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Plant Extracts / Oxidative Stress / Ginkgo biloba / Disease Models, Animal / Alzheimer Disease / Hippocampus / Mitochondria / Neurons Limits: Animals Language: En Journal: PLoS One Journal subject: CIENCIA / MEDICINA Year: 2024 Document type: Article Affiliation country: Country of publication:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Plant Extracts / Oxidative Stress / Ginkgo biloba / Disease Models, Animal / Alzheimer Disease / Hippocampus / Mitochondria / Neurons Limits: Animals Language: En Journal: PLoS One Journal subject: CIENCIA / MEDICINA Year: 2024 Document type: Article Affiliation country: Country of publication: