Effect of Luteoloside on 3T3-L1 Preadipocyte Differentiation and Lipid Metabolism

Objective: To study the effect and mechanism of luteoloside on the differentiation and lipid metabolism of 3T3-L1 preadipocytes. Methods: The cytotoxicity of different concentrations of luteoloside on 3T3-L1 preadipocyte was detected using methyl thiazolyl tetrazolium (MTT) assay. Cell differentiation was induced by the cocktail method, and lipid droplets were observed by oil red O staining. The contents of triglyceride and total cholesterol in differentiated cells, as well as the secretion of related inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-10, leptin (LEP) and Adiponectin (ADPN) were measured. The relative expression levels of peroxisome proliferators activated receptor (PPAR) γ, CCAAT-enhancer-binding proteins (C/EBP)-α, sterol regulatory element-binding protein 1 (SREBP1), PPARα, uncoupling protein 1 (UCP-1), and carnitine palmitoyltransferase 1 (CPT-1) were analyzed by Western blotting. Results: The survival rate of 3T3-L1 preadipocytes decreased with the increase in luteoloside concentration, being above 80% at luteoloside concentrations of 5–60 μg/mL. Treatment with luteoloside significantly inhibited the differentiation of 3T3-L1 preadipocytes and reduced lipid accumulation. Luteoloside down-regulated the contents of TC and TG, the secretion of TNF-α, IL-6 and LEP, but up-regulated the secretion of IL-10 and ADPN. Luteoloside down-regulated the protein expression levels of PPARγ, C/EBP-α and SREBP1, but up-regulated those of PPARα, UCP-1 and CPT-1. Conclusion: Luteoloside can suppression the differentiation and lipid metabolism of 3T3-L1 preadipocytes. The mechanism may be that luteoloside down-regulates the protein expression of PPARγ, C/EBP-α, and SREBP1 to inhibit fat synthesis. Furthermore, it activates PPARα to upregulate downstream proteins and promote fat consumption. Luteoloside may also regulate the secretion of cytokines and promote cellular lipolysis, thus improving lipid metabolism imbalance.