White crystalline powder
leaves of Ginkgo biloba L.
()-Bilobalide/(5aR,8R,8aS,9R,10aS)-9-tert-Butyl-8,9-dihydroxydihydro-9H-furo[2,3-b]furo[3',2':2,3]cyclopenta[1,2-c]furan-2,4,7(3H,8H)-trione/BILOBALIDE/4H,5aH,9H-Furo[2,3-b]furo[3',2':2,3]cyclopenta[1,2-c]furan-2,4,7(3H,8H)-trione, 9-(1,1-dimethylethyl)dihydro-8,9-dihydroxy-, (3aS,5aR,8R,8aS,9R,10aS)-/(−)-Bilobalide from Ginkgo biloba leaves/(−)-Bilobalide/(-)-Bilobalide from Ginkgo biloba leaves/(3aS,5aR,8R,8aS,9R,10aS)-8,9-Dihydroxy-9-(2-methyl-2-propanyl)dihydro-9H-furo[2,3-b]furo[3',2':2,3]cyclopenta[1,2-c]furan-2,4,7(3H,8H)-trione
Methanol; Ethyl Acetate; Water
651.7±55.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:33570-04-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Bilobalide, the only sesquiterpene compound from Ginkgo biloba leaf, exhibits various beneficial pharmaceutical activities, such as antioxidant, anti-inflammation, and protective effects for the central nervous system. Several bioactive components extracted from Ginkgo biloba extract reportedly have the potential to attenuate lipid metabolism. However, the effect of bilobalide on lipid metabolism remains unclear. In this study, we used 3T3-L1 cells as the cell model to investigate the effect of bilobalide on adipogenesis. The results showed that bilobalide inhibited 3T3-L1 preadipocyte differentiation and intracellular lipid accumulation. Quantitative real-time PCR and western blotting results indicated that several specific adipogenic transcription factors and a few important adipogenesis-related genes were significantly down regulated on both mRNA and protein levels in bilobalide treatment groups. By contrast, the expression of some lipolytic genes, such as adipose triglyceride lipase, hormone-sensitive lipase (HSL), and carnitine palmitoyltransferase-1α, were all up-regulated by bilobalide treatment, and the phosphorylation of AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase 1, and HSL were stimulated. Furthermore, bilobalide treatment partially restored AMPK activity following its blockade by compound C (dorsomorphin). These results suggested that bilobalide inhibited adipogenesis and promoted lipolysis in 3T3-L1 cells by activating the AMPK signaling pathway.
3T3-L1 cell; AMPK pathway; bilobalide; lipid metabolism.
Bilobalide Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway
Su Bu 1 , Chun Ying Yuan 2 , Quan Xue 3 , Ying Chen 4 , Fuliang Cao 5
2019 Sep 27
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system characterized by recurrent and progressive demyelination, neuroinflammation and oligodendrocyte loss. The cuprizone (CPZ) model is characterized by primary and reversible demyelination, accompanied by oligodendrocyte loss and neuroinflammation. In the current study, we explored the efficiency of Bilobalide in the demyelination and remyelination. The results demonstrate that Bilobalide improved behavioral abnormality and promoted remyelination in the corpus callosum by using Luxol Fast Blue, Black Gold II and myelin basic protein (MBP) staining. We for the first time found that CPZ caused the splenic atrophy and induced the formation of myelin oligodendrocyte glycoprotein (MOG) antibody, which was attenuated by Bilobalide. Thus, Bilobalide decreased the loss of O4+ oligodendrocytes possibly through MOG antibody-dependent cell cytotoxicity. Bilobalide also prevented the infiltration of CD4+ T cells, CD68+ macrophages and B220+ B cells within the brain, and reduced the inflammatory microenvironment mediated with Iba1+iNOS+ and Iba1+NF-kB+ microglia after CPZ challenge, accompanied by the inhibition of IL-1β and IL-6 in the brain. These results identify a potent therapeutic efficiency for Bilobalide and highlight clear pleiotropic effects of the compound beyond specific autoantibody and inflammatory microenvironment in CPZ-mediated demyelination.
3T3-L1 cell; AMPK pathway; bilobalide; lipid metabolism.
Protective and Therapeutic Role of Bilobalide in Cuprizone-Induced Demyelination
Ruo-Xuan Sui 1 , Qiang Miao 1 , Jing Wang 2 , Qing Wang 1 , Li-Juan Song 1 , Jing-Wen Yu 3 , Liang Cao 4 , Wei Xiao 4 , Bao-Guo Xiao 5 , Cun-Gen Ma 6
The accumulation of aggregated forms of the α-Synuclein (α-Syn) is associated with the pathogenesis of Parkinson’s disease (PD), a chronic progressive neurodegenerative disorder. Extensive evidences have shown the promising effects of Ginkgo biloba consumption on motor activity after PD. However, the mechanisms underline the α-Syn-induced cell damage and whether ginkgolides exert neuroprotection against this injury are unclear. Here we showed that aggregated recombinant human α-Syn, but not α-Syn monomers, triggered cell injury in cultured human neuroblastoma cell line SH-SY5Y in an apoptosis way by using flow cytometry and western blot assay. Moreover, pre-treatment with the Ginkgolide B (GB) or Bilobalide (BB) protected SH-SY5Y cells against α-Syn-induced cell viability decreases, and reduced cell apoptosis after aggregated α-Syn stimulation. Together, we firstly find that aggregated α-Syn induced cell apoptosis and GB and BB may attenuate aggregated α-Syn-induced cell apoptosis, which gives us an insight into the novel therapy for PD in future.
Aggregates; Apoptosis; Bilobalide; Ginkgolide B; α-Synuclein
Ginkgolide B and Bilobalide Ameliorate Neural Cell Apoptosis in α-Synuclein Aggregates
Jun Hua 1 , Nuo Yin 2 , Beibei Yang 3 , Ji Zhang 4 , Jianhua Ding 2 , Yi Fan 5 , Gang Hu 6
Bilobalide is a biologically active terpenic trilactone present in Ginkgo biloba. An increasing number of studies have demonstrated its neuroprotective effects.IC50 Value: 3.33 (pIC50 Value) Target: neuroprotectivein vitro: Inhibition by BB and GB was abolished in mutant receptors containing T6'S and S12'A substitutions, but their potencies were enhanced (42- and 125-fold, respectively) in S2'A mutant receptors . BB enhanced the secretion of α-secretase-cleaved soluble amyloid precursor protein (sAPPα, a by-product of non-amyloidogenic processing of APP) and decreased the β amyloid protein (Aβ, a by-product of amyloidogenic processing of APP) via PI3K-dependent pathway .in vivo: Oral administration of bilobalide (10-30 mg/kg) significantly inhibited thermal hyperalgesia in response to carrageenan, capsaicin and paw incision, independent of dose, with an efficacy similar to that of diclofenac. In the carrageenan model, mechanical hypersensitivity and paw oedema were also significantly reduced after treatment with bilobalide (10-30 mg/kg) . BB(4 and 8 mg/kg) significantly protected VD rats against cognitive deficits in the Morris water maze. Biochemical assessment showed that BB (4 and 8 mg/kg) increased superoxide dismutase (SOD) activity and glutathione (GSH) content, and decreased nitric oxide synthase (NOS) activity and malondialdehyde (MDA) content .Clinical trial: N/A