2. Academic Validation
  3. Ginsenoside CK modulates glucose metabolism via PPARγ to ameliorate SCOP-induced cognitive dysfunction

Ginsenoside CK modulates glucose metabolism via PPARγ to ameliorate SCOP-induced cognitive dysfunction

  • Metab Brain Dis. 2025 Apr 3;40(4):168. doi: 10.1007/s11011-025-01596-9.
Na Li 1 2,  Xingyu Fang 1,  Hui Li 3,  Jian Liu 1,  Nan Chen 1,  Xiaohui Zhao 1,  Qing Yang 4,  Xijun Chen 5
Affiliations

Affiliations

  • 1 Jinlin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, Jilin, P.R. China.
  • 2 Healthy Longevity Translational Research Program, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 119077, Singapore.
  • 3 Qian Wei Hospital of Jilin Province, Changchun, 130117, Jilin, P.R. China.
  • 4 Jinlin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, 130117, Jilin, P.R. China. qingyangyg@163.com.
  • 5 Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, P.R. China. chenxijun@wmu.edu.cn.
PMID: 40178645 DOI: 10.1007/s11011-025-01596-9
Abstract

Ginsenoside compound K (CK) exhibits neuroprotective properties; however, the underlying mechanisms behind these effects have not been investigated thoroughly. CK is the primary active compound derived from ginseng and is metabolized in the gut. It enhances neuronal function by modulating the gut microflora. Therefore, the present study aimed to elucidate the mechanism through which CK enhances cognitive function, employing gut microbiome and microarray analyses. The results revealed that CK upregulated the expression of Peroxisome Proliferator-activated Receptor gamma (PPARγ), suppressed Amyloid-β (Aβ) aggregation in hippocampal neurons, and influenced the expression of cyclin-dependent kinase-5 (CDK5), (including Insulin Receptor substrate 2) IRS2, insulin-degrading enzyme (IDE), glycogen synthase kinase-3 beta (GSK-3β), glucose transporter type 1 (GLUT1), and glucose transporter type 3 (GLUT3) proteins. These proteins play crucial roles in regulating brain glucose metabolism, increasing neuronal energy, and reducing neuronal Apoptosis, thereby ameliorating cognitive impairment in mice.

Keywords

Cognitive impairment; Ginsenoside CK; Glucose metabolism; PPARγ.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-16578
    99.79%, PPARγ Antagonist