The present study demonstrates a novel herbal formulation LI85008F inhibiting adipocyte differentiation and potentiates lipolysis in 3T3-L1 mouse adipocytes. LI85008F is formulated by combining extracts of three India...The present study demonstrates a novel herbal formulation LI85008F inhibiting adipocyte differentiation and potentiates lipolysis in 3T3-L1 mouse adipocytes. LI85008F is formulated by combining extracts of three Indian herbs Moringa oleifera, Murraya koenigii and Curcuma longa. Oil red O staining of 3T3-L1 adipocytes reveals that LI85008F is a synergistic formulation that inhibits adipocyte differentiation in a dose dependent manner and concurrently down regulates the key adipogenic transcription factors Peroxisome Proliferator-Activated Receptor gamma (PPAR) and CCAAT/enhancer binding protein α (C/EBP). LI85008F confers significant reductions in intracellular triglyceride content in a dose dependent manner. Evidence suggests that LI85008F antagonizes PPAR through Ser112 phosphorylation via MAPK/ERK activation. Immunoblot analyses reveal that LI85008F treatment also down regulates the protein expressions of key PPAR responsive gene products such as Adipocyte differentiation related protein (ADRP), CD36, Adipocyte specific binding protein 2 (aP2) and perilipin. In differentiated adipocytes culture, LI85008F treatment results in significantly (p = 0.0169) increased lipolysis as measured by the release of glycerol. LI85008F does not exhibit cytotoxic effect on adipocytes. Taken together, the results suggest that LI85008F inhibits lipogenesis in adipocytes and concurrently antagonizes PPAR? and other lipogenic factors and in addition, potentiates triglyceride mobilization from the fat cells or enhances lipolysis.展开更多
文摘The present study demonstrates a novel herbal formulation LI85008F inhibiting adipocyte differentiation and potentiates lipolysis in 3T3-L1 mouse adipocytes. LI85008F is formulated by combining extracts of three Indian herbs Moringa oleifera, Murraya koenigii and Curcuma longa. Oil red O staining of 3T3-L1 adipocytes reveals that LI85008F is a synergistic formulation that inhibits adipocyte differentiation in a dose dependent manner and concurrently down regulates the key adipogenic transcription factors Peroxisome Proliferator-Activated Receptor gamma (PPAR) and CCAAT/enhancer binding protein α (C/EBP). LI85008F confers significant reductions in intracellular triglyceride content in a dose dependent manner. Evidence suggests that LI85008F antagonizes PPAR through Ser112 phosphorylation via MAPK/ERK activation. Immunoblot analyses reveal that LI85008F treatment also down regulates the protein expressions of key PPAR responsive gene products such as Adipocyte differentiation related protein (ADRP), CD36, Adipocyte specific binding protein 2 (aP2) and perilipin. In differentiated adipocytes culture, LI85008F treatment results in significantly (p = 0.0169) increased lipolysis as measured by the release of glycerol. LI85008F does not exhibit cytotoxic effect on adipocytes. Taken together, the results suggest that LI85008F inhibits lipogenesis in adipocytes and concurrently antagonizes PPAR? and other lipogenic factors and in addition, potentiates triglyceride mobilization from the fat cells or enhances lipolysis.
