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Corresponding Author(s)

覃思(1981—),男,湖南农业大学教授,博士。E-mail:qinsiman@hunau.edu.cn

Abstract

[Objective] To explore the mechanism by which procyanidin B2 (PB2) intervenes in inflammation and insulin resistance (IR) through multi-target modulation. [Methods] The potential of PB 2 in diabetes prevention was evaluated via in vitro antioxidant assays, and molecular biology techniques were used to reveal the regulatory effect of PB 2 on the NF-κB inflammatory signaling pathway during the progression of IR. [Results] PB2 significantly reduced reactive oxygen species (ROS) levels in HepG 2 cells by scavenging free radicals and inhibited the expression of inflammatory factors IL-6, IL-1β, and TNF-α. By suppressing the JNK/NF-κB signaling cascade, PB2 blocked excessive ROS production, thereby restoring intracellular redox homeostasis and ultimately improving insulin resistance. [Conclusion] PB2 can regulate glucose metabolism and antagonize inflammatory responses by modulating redox balance and inflammatory signaling pathways.

Publication Date

9-25-2025

First Page

143

Last Page

148

DOI

10.13652/j.spjx.1003.5788.2025.80395

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