product name Ginkgolide B
Description: Ginkgolide B (also known as BN52021) is a PAFR antagonist with IC50 of 3.6 μM. Ginkgolide B potently inhibits a platelet-activating factor (PAF) receptor. Treatment of PMN with ginkgolide B (0.5 μM -12 μM) stimulates a rapid and weak production of reactive oxygen species determined by chemiluminescence. Ginkgolide B potentiates the CL response induced by fMet-Leu-Phe and zymosan. Ginkgolide B induces cyst cell differentiation and alteres the Ras/MAPK signaling pathway.
References: Biochem Pharmacol. 1987 Sep 1;36(17):2749-52; Am J Physiol Renal Physiol. 2012 May 15;302(10):F1234-42.
424.4
Formula
C20H24O10
CAS No.
15291-77-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 85 mg/mL (200.3 mM)
Water: <1 mg/mL
Ethanol: 2 mg/mL (4.9 mM)
Solubility (In vivo)
30% Propylene glycol, 5% Tween 80, 65% D5W: 10mg/mL
Synonyms
BN52021
other peoduct :
| In Vitro |
In vitro activity: Ginkgolide B potently inhibits a platelet-activating factor (PAF) receptor. Treatment of PMN with ginkgolide B (0.5 μM -12 μM) stimulates a rapid and weak production of reactive oxygen species determined by chemiluminescence. Ginkgolide B potentiates the CL response induced by fMet-Leu-Phe and zymosan. Ginkgolide B induces cyst cell differentiation and alteres the Ras/MAPK signaling pathway. Ginkgolide B promotes the proliferation and endothelial gene expression, and markedly enhances vascular endothelial growth factor-induced migration response and the capability to incorporate into the vascular networks in EPCs. Ginkgolide B protects EPCs from H2O2-induced cell death. Ginkgolide B induces the phosphorylation of eNOS, Akt and p38, which in turn promotes cell proliferation and function. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Ginkgolide B (2 μM) significantly inhibits MDCK cyst formation dose dependently, with up to 69% reduction. Ginkgolide B also significantly inhibits cyst enlargement in the MDCK cyst model, embryonic kidney cyst model, and PKD mouse model. Preischemic application of Ginkgolide B (50 mg/kg p.o.) significantly reduces neuronal damage. 30 minutes of pretreatment with Ginkgolide B (100 mg/kg, s. c.) reduces the infarct area in the mouse model of focal ischemia. In primary cultures of hippocampal neurons and astrocytes from neonatal rats, Ginkgolide B (1 μM) protects the neurons against damage caused by glutamate. Ginkgolide B (100 μM) reduces apoptotic damage induced by staurosporine. In pentobarbitone or ethyl carbamate-anaesthetized animals, Ginkgolide B (1 mg/kg i.v. or 10 mg/kg p.o.) inhibits bronchoconstriction, the hematocrit increase and the accompanying thrombopenia and leukopenia induced by PAF-acether (33 ng/kg–100 ng/kg). Ginkgolide B at a dose of 3 mg/kg reduces the bronchoconstriction induced by aerosolized PAF-acether. Ginkgolide B at a dose of 300 μM also inhibits the superoxide production by PAF-acether-stimulated alveolar macrophages. Ginkgolide B blocks the formation of thromboxane-triggered by PAF-acether (100 ng) injected into perfused lung.Pretreatment of parenchyma lung strips with Ginkgolide B (100 μM) partially inhibits the contraction induced by PAF-acether (0.1 μM) and suppresses the accompanying release of thromboxane. Ginkgolide B inhibits the maturation of ischemic injury. Ginkgolide B treatment reveals marked reduction in infarction volume, brain edema and neurological deficits. Ginkgolide B also inhibitsischemia/reperfusion (I/R) induced NF-κB, microglia activation and production of pro-inflammatory cytokines. Ginkgolide B reducesBax protein levels and increases Bcl-2 protein levels in the post-ischemic brains. Ginkgolide B attenuates platelet aggregation and inhibits phosphatidylinositol 3 kinase (PI3K) activation and Akt phosphorylation in thrombin- and collagen-activated platelets.Ginkgolide B decreases plasma PF4 and RANTES levels in ApoE−/− mice.Ginkgolide B diminishes P-selectin, PF4, RANTES, and CD40L expression in aortic plaque in ApoE−/− mice.Moreover, ginkgolide B suppresses macrophage and vascular cell adhesion protein 1 (VCAM-1) expression in aorta lesions in ApoE−/− mice. |
| Animal model | Eight-week-old male ApoE−/− mice |
| Formulation & Dosage | Dissolved in PBS; 0.6 mg/day; Intragastric administration |
| References | Biochem Pharmacol. 1987 Sep 1;36(17):2749-52; Am J Physiol Renal Physiol. 2012 May 15;302(10):F1234-42. |
