Abstract

Objectives : The present study was designed to investigate effects and molecular mechanisms of Atractylodes macrocephala Koidzumi extracts(AMK) on the improvement of adipocyte dysfunction induced by TNF-α in 3T3-L1 adipocytes. We examined whether AMK could directly influence the inflammation and insulin resistance in 3T3-L1 adipocytes. Methods : Potential roles of AMK in the lipolysis, production of inflammatory adipokines and ROS, expression and phosphorylation of ERK, JNK, and IκBα protein, and expression of PPARγ and C/EBPα were investigated in this study. Results : Our data demonstrated that TNF-α significantly increased lipolysis, levels of MCP-1, IL-6, and ROS and phosphorylation of ERK, JNK, and IκBα protein, while TNFα reduced the expression of PPARγ and C/EBPα in adipocytes, suggesting that TNF-α induced a condition with the occurrence of inflammation and insulin resistance. Those alterations induced by TNF-α were prevented by the treatment of AMK. AMK down-regulated the phosphorylation of ERK, JNK, and IκBα protein and up-regulated the expression of PPARγ and C/EBPα on TNF-α-induced inflammation and insulin resistance. Conclusions : Thus, our results indicate that AMK can be used to prevent from the TNF-α-induced adipocyte dysfunction through MAPK, NFκB and PPARγ pathways.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call