科研之友
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摘要
Background: The rising incidence of metabolic diseases due to chronic inflammation in the adipose tissue has been attributed to factors such as high fat diet (HFD). Previous studies have demonstrated that the total saponins from Panax japonicus (TSPJ) can reduce HFD-induced adipocyte inflammation, but the underlying mechanism remains unclear. In this work, we explored the molecular mechanism by which TSPJ reduces inflammation response in adipocytes. @@@ Methods: We first established C57BL/6 mouse and 3T3-L1 adipocyte models. Lentiviruses packaged with the plasmids were injected into mice through the tail vein or into adipocytes to generate the in vivo and in vitro models with miR155 knockdown and overexpression. The mice were fed with HFD to trigger inflammation and administered TSPJ (25 mg/kg center dot d and 75 mg/kg center dot d) by gavage. The adipocytes were treated with palmitic acid (PA) to trigger inflammation response, then treated with TSPJ (25 mu g/ml and 50 mu g/ml). Finally, the expression of miR155, inflammatory factors, SOCS1, and NFKB pathway-related proteins was explored. @@@ Results: TSPJ significantly inhibited the expression of inflammation-related genes and the miR155 expression in adipocytes both in vitro and in vivo. The dual luciferase reporter gene assay revealed that miR155 mediated the downregulation of SOCS1. TSPJ significantly inhibited and upregulated the phosphorylation of the NFKB protein and the SOCS1 proteins, respectively. @@@ Conclusion: TSPJ inhibits miR155 to upregulate the SOCS1 expression, which subsequently inhibits the NFKB signaling pathway, thereby mitigating the inflammatory response in the adipocytes of HFD mice.
