Title:Astragaloside IV Regulates Insulin Resistance and Inflammatory Response
of Adipocytes via Modulating MIR-21/PTEN/PI3K/AKT Signaling
Volume: 23
Issue: 12
Author(s): Xuxi Guo, Taoqing Yin, Dongni Chen, Shuai Xu, Renqun Ye*Yue Zhang*
Affiliation:
- Department of Endocrinology, Shenzhen Bao’an Traditional Chinese Medicine Hospital, The Affiliated Hospital of
Guangzhou University of Chinese Medicine, Shenzhen, China
- Department of Endocrinology, Shenzhen Bao’an Traditional Chinese Medicine Hospital, The Affiliated Hospital of
Guangzhou University of Chinese Medicine, Shenzhen, China
Keywords:
T2DM, AS-IV, insulin resistance, inflammation, adipocytes, miR-21.
Abstract:
Background: The progression of Type 2 Diabetes Mellitus (T2DM) can lead to various
complications. Compounds derived from natural products have been found to be effective in combatting
T2DM. This study aimed to investigate the effects of Astragaloside IV (AS-IV) on insulin
resistance and the inflammatory response of adipocytes. The study also aimed to determine the
downstream signaling pathways involved.
Materials and Methods: The glucose consumption of adipocytes was assessed using a glucose
assay kit. qRT-PCR, Western blot, and ELISA assays were used to measure mRNA and protein
levels. The interaction between miR-21 and PTEN was assessed using a Dual-luciferase reporter
assay.
Results: The results showed that AS-IV increased glucose consumption and the expression of
GLUT-4 in adipocytes with insulin resistance in a concentration-dependent manner. However, ASIV
decreased the protein levels of TNF-α and IL-6 in these cells. Additionally, AS-IV up-regulated
miR-21 expression in adipocytes with insulin resistance in a concentration-dependent manner. Furthermore,
miR-21 overexpression increased glucose consumption and GLUT-4 expression but decreased
TNF-α and IL-6 protein levels in adipocytes. Conversely, miR-21 inhibition attenuated the
AS-IV-induced increase in glucose consumption and GLUT-4 expression and the decrease in TNF-
α and IL-6 protein levels in adipocytes. MiR-21 also inversely regulated PTEN in adipocytes, and
PTEN overexpression had effects similar to miR-21 inhibition in AS-IV-treated adipocytes. Finally,
AS-IV up-regulated p-PI3K and p-AKT protein expression in adipocytes, which was attenuated
by miR-21 inhibition.
Conclusion: The study concluded that AS-IV attenuated insulin resistance and the inflammatory
response in adipocytes. The mechanistic studies indicated that AS-IV modulated the miR-
21/PTEN/PI3K/AKT signaling in adipocytes to exert these effects.
