Ginsenoside Rb1 inhibits free fatty acids-induced oxidative stress and inflammation in 3T3-L1 adipocytes

• DOI: 10.3892/mmr.2017.7710
• Publication Date: 2017-10-04T06:53:54Z
• Authors: Min Wang; Yanming Chen; Zhaojun Xiong; Shujie Yu; Bin Zhou; Yesheng Ling; Zhenda Zheng; Guangyao Shi; Yongxiang Wu; Xiaoxian Qian
• Keywords: Proinflammatory cytokine

Free fatty acids (FFAs) increase in visceral fat and are inferred to be one of the underlying inducers adipose tissue inflammation. In our previous study, it was demonstrated that ginsenoside Rb1 stimulates endothelial nitric oxide synthase (eNOS) Sirtuin 1 protect against cell senescence. present 3T3‑L1 adipocytes were exposed 0.5 mM FFAs with or without (10‑40 µM). Monocyte chemotactic protein‑1 (MCP‑1) interleukin‑6 (IL‑6) secretion measured using ELISA. Tumor necrosis factor‑α (TNF‑α) expression nuclear factor‑κB (NF‑κB) p65 phosphorylation detected western blot analysis. Oxidative stress determined via measuring intracellular reactive oxygen species (ROS) (NO) production. The results MCP‑1 IL‑6 secretion, as well TNF‑α expression, significantly increased following FFA treatment, which attenuated by a dose‑dependent manner. Furthermore, FFA‑induced NF‑κB phosphorylation, suggesting inhibitory effect on inflammatory cytokines partially mediated through blockade phosphorylation. Further experiments ameliorated ROS generation NO reduction upregulation superoxide dismutase 2 eNOS expression. Taken together, these demonstrate proinflammatory pro‑oxidant effects adipocytes, effectively Rb1. Suppression responses oxidative may novel mechanism for attenuating adipocyte dysfunction.