ZHU Qing, WEN Tian-yan, YANG Dao-ju, et al. Effect and Molecular Mechanisms of Xiaozhi Decoction on NASH Cell Model Induced by FFA in HepG2 Cell[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 109-115.
DOI:
ZHU Qing, WEN Tian-yan, YANG Dao-ju, et al. Effect and Molecular Mechanisms of Xiaozhi Decoction on NASH Cell Model Induced by FFA in HepG2 Cell[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(23): 109-115. DOI: 10.13422/j.cnki.syfjx.2017230109.
Effect and Molecular Mechanisms of Xiaozhi Decoction on NASH Cell Model Induced by FFA in HepG2 Cell
Objective: To investigate the effect and mechanism of Xiaozhi decoction on free fatty acids (FFA)-induced non-alcoholic steatohepatitis (NASH) cell model. Method: The NASH model in HepG2 cells was induced by 0.5 μmol·L-1 FFA. The NASH cell models were established by different concentrations of Xiaozhi decoction and fenofibrate. Oil red O staining was used to observe the content of lipid droplets. Cell supernatant (nuclear factor-κ-gene binding) NF-κB p65
Phospho-insulin receptor substrate[Phospho-IRS-1 (Ser307)] and insulin receptor substrate-1 (IRS-1) protein were detected by Western blot. Result: The contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6(IL-6) in the supernatant fluid of the model group were significantly higher than those in control group (P<0.01). Meanwhile
the expression of IRS-1 was reduced (P<0.05)
while the levels of IKKβ
p-IKKα/β (Ser176/180) and IRS-1(Ser307) phosphorylation and nuclear translocation of NF-κB p65 protein were increased in the model group (P<0.01). The expressions of IKKα/β (Ser176/180) and IRS-1 (Ser307) phosphorylation and nuclear translocation of NF-κB p65 protein in each dose group were decreased (P<0.01)
especially in high-dose Xiaozhi decoction. The protein expression of IRS-1 was significantly increased (P<0.05) in control group. Conclusion: Xiaozhi decoction can improve lipid deposition and inflammatory reaction in NASH cell model induced by FFA. The mechanism may be related to the inhibition of intracellular IKKα/β (Ser176/180) and IRS-1 (Ser307) phosphorylation and IKKβ