Abstract
The present study has examined the effect of procyanidin A1 on insulin resistance and oxidative stress in palmitic acid treated HepG2 cells. The HepG2 cells were pretreated with procyanidin A1 and then with palmitic acid. The cell viability and the levels of catalase, superoxide dismutase, glutathione peroxidase, and reactive oxygen were used to assess oxidative stress. Treatment with palmitic acid significantly reduced cell viability that was alleviated by cotreatment with procyanidin A1. In addition, procyanidin A1 restored the palmitic acid induced insulin resistance and oxidative stress in the HepG2 cells. Furthermore, inactivation of P38 MAPK and JNK signaling pathways was closely associated with the procyanidin A1-regulated resistance and oxidative stress in palmitic acid treated HepG2 cells. In conclusion, procyanidin A1 inhibits insulin resistance and oxidative stress in palmitic acid treated HepG2 cells by regulating the P38 MAPK and JNK signaling pathways.
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