Paeoniflorin suppresses lipid accumulation and alleviates insulin resistance by regulating the Rho kinase/IRS-1 pathway in palmitate-induced HepG2Cells

Abstract

In this study, we evaluated the effects of paeoniflorin (PF) on palmitate (PA)-induced insulin resistance and explored the potential molecular mechanisms in HepG2 cells. HepG2 cells were pre-treated with 3μM, 30μM, or 100μM PF for 1h followed by immediate stimulation with 0.25mM palmitate for 24h to induce hepatic steatosis. PF treatment could decrease PA-induced intracellular lipid deposition via inhibiting de novo lipid synthesis. PF treatment also restored insulin sensitivity by suppressing the activation of Rho kinase (ROCK) and the expression of serine phosphorylation of insulin receptor substrate (IRS)-1, thereby promoting Akt and glycogen synthase kinase (GSK)-3β phosphorylation. These results suggest that PF alleviates PA-induced hepatic steatosis and insulin resistance in HepG2 cells. Furthermore, the effect of PF may be associated with its role in inhibiting de novo lipid synthesis and in regulating the ROCK/IRS/Akt signalling pathways.