GRg1 Ameliorates Insulin Resistance Through Activation of the PI3K/AKT/GSK-3β Pathway in HepG2 Cells
Xunjun Shen1, Yamei Jin1★, Yuting Chen1, Huadi Yang2★ Corresponding author
- 1Department of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, CHINA.
- 2Department of Gynecology and Obstetrics, The First Affiliated Hospital of Zhejiang Chinese Medical University, (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China, CHINA.
CORRESPONDENCE
Yamei Jin
Department of Endocrinology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, CHINA.
Received: 06-04-2023; Accepted: 03-08-2023.
Volume 20, Issue 1 · pp. 257–267 · PUBLISHED 2024 · DOI: 10.1177/09731296231198284
View on Pharmacogn. Mag. original site ↗
ABSTRACT
Background: Insulin resistance (IR) is a pathological state closely associated with various diseases, with hepatic insulin resistance playing a pivotal role. Insulin resistance can be improved by Ginsenoside Rg1 (GRg1), which is known as one of the most biologically active compounds found in ginseng. Nevertheless, the precise role and mechanisms of GRg1 in ameliorating hepatic insulin resistance are still unknown. Objectives: We wanted to demonstrate the impact of GRg1 on hepatic insulin resistance and explore the underlying mechanisms in our work. Materials and Methods: We mimicked insulin resistance conditions by culturing HepG2 cells in 30 mM glucose for 24 h. The effects of GRg1 on cellular glucose consumption and the key kinases of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK-3β) pathway were evaluated. To assess if the PI3K/AKT/GSK-3β pathway is crucial for GRg1’s protective effect against insulin resistance, the compound LY294002, which inhibits PI3K, was employed. Results: In HepG2 cells, GRg1 markedly increased glucose uptake while exhibiting no cytotoxicity. Additionally, GRg1 activated the PI3K/AKT/GSK-3β pathway, as indicated by the increased phosphorylation of insulin receptor substrates-1 (IRS-1), AKT, and GSK-3β. Treatment with LY294002 significantly reversed the promotive effects of GRg1 on cellular glucose consumption and PI3K/AKT/GSK-3β pathway activation. Conclusion: Taken together, our present study revealed GRg1 exerted a protective effect against hepatic insulin resistance induced by high glucose through PI3K/AKT/GSK-3β pathway, suggesting its potential as a beneficial therapeutic medication.
KEYWORDS
REFERENCES
As publishedShowing references and in-text citations exactly as published.
Cite this article
SELECT FORMAT
Shen, X., Jin, Y., Chen, Y., & Yang, H. (2024). GRg1 Ameliorates Insulin Resistance Through Activation of the PI3K/AKT/GSK-3β Pathway in HepG2 Cells. Pharmacognosy Magazine, 20(1), 257–267. https://doi.org/10.1177/09731296231198284