Cell experiment:

3T3-L1 cells are treated with various concentrations of ginkgolide C in 96-well plates for 24 h. Cell viability is analyzed by the MTT assay. The culture medium is removed, and the cells are incubated with 100 μL MTT solution (5 mg/mL) for 4 h at 37℃. After plates are washed, isopropanol is added to dissolve formazone crystals, followed by absorbance detection with a spectrophotometer at 570 nm[1].

Ginkgolide C is a flavone isolated from Ginkgo biloba leaves, possessing multiple biological functions, such as decreasing platelet aggregation and ameliorating Alzheimer disease.

Ginkgolide C (3-100 μM) has no significant effect on 3T3-L1 cell viability, but suppresses adipogenesis in 3T3-L1 cells followling 24 h treatment. Ginkgolide C (10-100 μM) significantly suppresses lipid accumulation compared with the control group and also significantly promotes glycerol release in 3T3-L1 adipocytes. Ginkgolide C suppresses PPAR-α and PPAR-γ expression and decreases C/EBPα, C/EBPβ, and SREBP-1c expression in differentiated 3T3-L1 adipocytes. In addition, Ginkgolide C (3-100 μM) suppress adipogenesis-related protein (FAS, LPL, and aP2) and mRNA expression in a dose-dependent manner in differentiated 3T3-L1 adipocytes. Ginkgolide C (3-100 μM) also significantly promotes Sirt1 production and increases phosphorylation of AMPKα and ACC-1 in a concentration-dependent manner[1]. Ginkgolide C (1, 10, 50, 100, 500 mM) significantly reduces the collagen (10 mg/mL)-stimulated rat platelet aggregation in a dose-dependent manner. Ginkgolide C (50, 100 mM) causes pro-MMP-9 (92-kDa) to form an activated MMP-9 (86-kDa) in collagen-stimulated platelets[2].

References:
[1]. Liou CJ, et al. Ginkgolide C Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway. Evid Based Complement Alternat Med. 2015;2015:298635.
[2]. Ginkgolide C, et al. Ginkgolide C inhibits platelet aggregation in cAMP- and cGMP-dependent manner by activating MMP-9. Biol Pharm Bull. 2007 Dec;30(12):2340-4.