Silibinin Inhibits Adipogenesis and Induces Apoptosis in 3T3-L1 Adipocytes
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C/EBPβ and C/EBPδ are required for the initiation of adipogenesis and induce the expression of key adipogenic regulators, such as PPARγ and C/EBPα. In the present study, we have examined the effects of silibinin and its possible molecular mechanisms in regulating adipocyte differentiation and expression of C/ EBPβ and C/EBPδ in the early stage of adipogenesis. Silibinin statistically significantly inhibits intracellular lipid accumulation and the mRNA expression of various genes involved at different stages during adipogenesis. Silibinin also suppresses expression of lipoprotein lipase (LPL), fatty acid binding protein 4 (AP2), and adiponectin in 3T3-L1 adipocytes. Thus, the anti-adipogenic effect of silibinin seems to originate from the ability to inhibit the expression of C/EBPβ and C/EBPδ. Furthermore, silibinin decreases cell viability for differentiation period and induces apoptotic cell death through capspase-3 activation.
Abstract
C/EBPβ and C/EBPδ are required for the initiation of adipogenesis and induce the expression of key adipogenic regulators, such as PPARγ and C/EBPα. In the present study, we have examined the effects of silibinin and its possible molecular mechanisms in regulating adipocyte differentiation and expression of C/ EBPβ and C/EBPδ in the early stage of adipogenesis. Silibinin statistically significantly inhibits intracellular lipid accumulation and the mRNA expression of various genes involved at different stages during adipogenesis. Silibinin also suppresses expression of lipoprotein lipase (LPL), fatty acid binding protein 4 (AP2), and adiponectin in 3T3-L1 adipocytes. Thus, the anti-adipogenic effect of silibinin seems to originate from the ability to inhibit the expression of C/EBPβ and C/EBPδ. Furthermore, silibinin decreases cell viability for differentiation period and induces apoptotic cell death through capspase-3 activation.
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