Effects and Mechanisms of Ginsenoside Rg1 on Free Fatty Acid Mediated Inflammation in NASH Cell Model
XIAO Qing, ZHANG Shujun, YANG Cheng, GAO Yue, XU Jing, ZHU Yali, HUANG Wenxiang*
This work was to investigate the effect of ginsenoside Rg1 on inflammation in NASH (non-alcoholic steatohepatitis) cell model and its molecular mechanism. HepG2 cells and L02 cells were treated with 1 mmol/L FFA (free fatty acid) for 24 h, and then treated with 20 μg/mL or 40 μg/mL ginsenoside Rg1 for 6 h. The control group, model group, low-dose Rg1 group and high-dose Rg1 group were set. The ALT (alanine aminotransferase) and AST (aspartate aminotransferase) in supernatant were detected by automatic biochemical analyzer. IL-1β, IL-6, TNF-α in supernatant were detected with ELISA (enzyme-linked immunosorbent assay). RT-qPCR and Western blot were used to detect alterations of genes and proteins related to NF-κB pathway. Immunofluorescence was used to demonstrate NF-κB P65 nuclear translocation. and Western blot was used to detect the expression of NF-κB P65 protein in the cytoplasm and nucleus of each group. Compared with the control group, the inflammatory cytokines in supernatant of the model group were significantly increased (P<0.05). Rg1 could decrease the expressions of inflammatory indicators (P<0.05). Rg1 could down-regulate FFA activated NF-κB phosphorylation, translocation of NF-κB P65 from cytoplasm to nucleus, and the downstream target genes of NF-κB, including IL-1β, IL-6 and TNF-α (P<0.05). Rg1 might alleviate FFA mediated inflammation in NASH cell model through inhibiting NF-κB activation, which provided a possible target for NASH treatment.
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