cInvestigating the protective effects of ginsenoside CK against oxidative stress-induced neuronal damage by 1H-NMR-based metabolomics

Genomics, Neuroscience
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Na Li# Changchun University of Chinese Medicine, Changchun, China

Yanhong Zhang Changchun University of Chinese Medicine, Changchun, China

Jingwei Lv Changchun University of Chinese Medicine, Changchun, China

Dazhong Sun Guangzhou University of Chinese Medicine, Guangzhou, China

Jianan Lin Changchun University of Chinese Medicine, Changchun, China

Qihang Pang Changchun University of Chinese Medicine, Changchun, China

Hui Li Department of General Surgery, Qian Wei Hospital of Jilin Province, Changchun, China

Zhanhong Cao Changchun University of Chinese Medicine, Changchun, China

Yaxin Liu Changchun University of Chinese Medicine, Changchun, China

Zhen Li Changchun University of Chinese Medicine, Changchun, China

Xingyu Fang Changchun University of Chinese Medicine, Changchun, China

Dianyu Li Changchun University of Chinese Medicine, Changchun, China

Haonan Bai Changchun University of Chinese Medicine, Changchun, China

Yu An Changchun University of Chinese Medicine, Changchun, China

Junjie Jiang Changchun University of Chinese Medicine, Changchun, China

Rui Zhang Changchun University of Chinese Medicine, Changchun, China

Qing Yang* Changchun University of Chinese Medicine, Changchun, China


Abstract

Oxidative stress is an important pathogenic mechanism in degenerative diseases such as Alzheimer's disease (AD). Although ginsenoside compound K (CK) is protective against neuronal oxidative damage, the underlying mechanism remains to be understood. In this study, the protective effects of ginsenoside CK against hydrogen peroxide-induced oxidative stress damage in HT22 cells were investigated by 1H nuclear magnetic resonance (1H-NMR)-based metabolomics. The optimal CK concentration for reducing oxidative stress damage in nerves was determined using the MTT. CK (8 μM) significantly increased the HT22 cell survival rate after the model was established. Cell lysates were subjected to 1H-NMR metabolomics, western blotting, and ATP assays for verification. Metabolic perturbation occurred in HT22 cells in the model group but not in the control group. Twenty biomarkers were identified in this study and used to analyze metabolic pathways. CK reversed metabolic changes in HT22 cells by altering taurine, glutamate, glycine, and glutathione metabolism. Subsequently, CK increased ATP content and expression of components of the PI3K/AKT signaling pathway in HT22 cells. These findings demonstrated CK can prevent oxidative stress damage and protect nerves by regulating energy metabolism pathways, such as taurine and glutamate metabolism and other amino acid metabolism pathways, providing a rationale for CK in AD.
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