Bilobalide possesses anticonvulsant, insecticidal, and cardioprotective effects. Bilobalide exerts protective and trophic effects on neurons, the PI3K/Akt pathway may be involved in the protective effects of bilobalide; it also can protect PC12 cells from A beta 25-35-induced cytotoxicity, it dose-dependently attenuates the cytotoxic effect of A beta 25-35.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C)
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Acta Pharmacol Sin. 2000 Jan;21(1):75-9.
Protective effects of bilobalide on amyloid beta-peptide 25-35-induced PC12 cell cytotoxicity.[Pubmed: 11263252
To study the effect of bilobalide[(-)-Bilobalide], a terpene extracted from the leaves of Ginkgo biloba, on beta-amyloid peptide fragment 25-35 (A beta 25-35)-induced PC12 cell cytotoxicity.
METHODS AND RESULTS:
3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay were used to measure the viability of PC12 cells. Thiobarbituric acid-reactive substances were measured to determine lipid peroxidation of cells. Antioxidant enzymes in PC12 cells were detected. Treatment of PC12 cells with A beta 25-35 (100 mumol.L-1) for 24 h caused a great decrease in cell viability (P < 0.01 compared with control). Bilobalide[(-)-Bilobalide] 25-100 mumol.L-1 dose-dependently attenuated the cytotoxic effect of A beta 25-35. Bilobalide[(-)-Bilobalide] also inhibited A beta 25-35 (100 mumol.L-1)-induced elevation of lipid peroxidation and decline of antioxidant enzyme activities.
Bilobalide[(-)-Bilobalide] protected PC12 cells from A beta 25-35-induced cytotoxicity.
Eur J Pharmacol. 1999 Feb 19;367(2-3):165-73.
Effects of bilobalide on gamma-aminobutyric acid levels and glutamic acid decarboxylase in mouse brain.[Pubmed: 10078989
We have previously demonstrated that Bilobalide[(-)-Bilobalide] a constituent of the Ginkgo biloba extract, possesses anticonvulsant activity, and suggested that the mechanism of its anticonvulsant action involves modulation of y-aminobutyric acid (GABA)-related neuronal transmission.
METHODS AND RESULTS:
This study examined the effects of Bilobalide[(-)-Bilobalide] on the level of GABA and glutamate, the activity and the amount of glutamic acid decarboxylase (EC 220.127.116.11), and the function of GABA(A) receptors in the hippocampus, cerebral cortex and striatum of the mouse. GABA levels, glutamic acid decarboxylase activity, and the protein amount of 67 kDa glutamic acid decarboxylase in the hippocampus of mice treated withBilobalide[(-)-Bilobalide] (30 mg/kg, p.o., once a day for 4 days) were significantly higher than those in controls. However, there were no significant differences in glutamate levels or, the number and the dissociation constants of GABA(A) receptors in the hippocampus between control and bilobalide-treated mice.
These results suggest that the anticonvulsant effect of bilobalide is due to elevation of GABA levels, possibly through potentiation of glutamic acid decarboxylase activity and enhancement of the protein amount of 67 kDa glutamic acid decarboxylase by bilobalideBilobalide[(-)-Bilobalide].
Apoptosis. 2010 Jun;15(6):715-27.
Bilobalide prevents apoptosis through activation of the PI3K/Akt pathway in SH-SY5Y cells.[Pubmed: 20333467
Bilobalide[(-)-Bilobalide], a sesquiterpene trilactone constituent of Ginkgo biloba leaf extracts, has been proposed to exert protective and trophic effects on neurons. However, mechanisms underlying the protective effects of bilobalide [(-)-Bilobalide]remain unclear. Using human SH-SY5Y neuroblastoma cells and primary hippocampal neurons, this study investigated the neuroprotective effects of bilobalide[(-)-Bilobalide].
METHODS AND RESULTS:
We mimicked aging-associated neuronal impairments by applying external factors (beta amyloid protein (Abeta) 1-42, H(2)O(2) and serum deprivation) consequently inducing cell apoptosis. As markers for apoptosis, cell viability, DNA fragmentation, mitochondrial membrane potential and levels of cleaved caspase 3 were measured. We found that, bilobalide[(-)-Bilobalide] prevented Abeta 1-42-, H(2)O(2)- and serum deprivation-induced apoptosis. To better understand the neuroprotective effects of bilobalide[(-)-Bilobalide], we also tested the ability of bilobalide[(-)-Bilobalide] to modulate pro-survival signaling pathways such as protein kinase C (PKC), extracellular-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways. It was found that, bilobalide[(-)-Bilobalide] dose-dependently increased PI3K activity and levels of phosphorylated Akt (p-Akt Ser473 and Thr308), which could be maintained up to at least 2 h after bilobalide withdrawal in cells treated with or without Abeta 1-42, H(2)O(2) or serum-free medium. In addition, application of PI3K/Akt inhibitor LY294002 could abrogate both the protective effects of bilobalide[(-)-Bilobalide] against Abeta 1-42-, H(2)O(2)- and serum deprivation-induced apoptotic cell damage and bilobalide[(-)-Bilobalide]-induced increase in PI3K activity and levels of p-Akt (Ser473 and Thr308). In contrast, application of PKC inhibitor staurosporine (STS) did not affect the protective effects of bilobalide[(-)-Bilobalide]. Moreover, no change in levels of phosphorylated ERK1/2 (p-ERK1/2) was observed in bilobalide-treated cells.
These results further suggested that the PI3K/Akt pathway might be involved in the protective effects of bilobalide[(-)-Bilobalide]. Since modern technology allows production of purified bilobalide[(-)-Bilobalide] with high bioavailability, bilobalide[(-)-Bilobalide] may be useful in developing therapy for diseases involving age-associated neurodegeneration.
Biosci Rep. 2011 Oct 1; 31(Pt 5): 439–447.
Anti-ischaemic effects of bilobalide on neonatal rat cardiomyocytes and the involvement of the platelet-activating factor receptor[Pubmed: 21391918
Terpene trilactones from Ginkgo biloba have been investigated extensively for their antioxidant and anti-ischaemic activities on the brain and the heart, but the mechanisms of these effects remain unclear.
METHODS AND RESULTS:
For the present study, a terpenoid constituent from G. biloba, bilobalide[(-)-Bilobalide], was screened for protective effects on the ischaemic heart and the involvement of the PAFR [PAF (platelet-activating factor) receptor] and the enzyme that degrades PAF, PAF-AH (PAF acetylhydrolase) during hypoxia. The PAF pathway is supposed to play a role in hypoxia and its regulation may prevent or alleviate MI (myocardial infarction). Cardiomyocytes from neonatal rat hearts were cultured and treated with different concentrations of bilobalide[(-)-Bilobalide] (500-0.5 ng/ml). After being subjected to a hypoxic environment, the cells' viability was evaluated and proteins as well as RNA were extracted for analysis by Western blotting and RT-PCR (reverse transcription PCR) respectively.
With the MI model we tested for bilobalide[(-)-Bilobalide]'s cardioprotective effects and the involvement of PAFR and PAF-AH. Bilobalide ((-)-Bilobalide,5 ng/ml) significantly decreased the mortality of cells in a concentration-dependent way. mRNA expression of PAFR was up-regulated in hypoxic cells but in the groups treated with bilobalide[(-)-Bilobalide], its expression was down-regulated to the level of the normal control. In hypoxic tissue, PAFR protein expression was also up-regulated, but was reduced in the bilobalide ((-)-Bilobalide,10 mg/kg of body weight) treated group.
Our results indicate that PAF and its receptor may be involved in the cellular response of cardiomyocytes to hypoxia and that bilobalide may interact with this receptor to exert its cardioprotective effects.
The Korean Society of Pesticide Science,2001,5(1):24-9.
Insecticidal Activities of Bilobalide from Ginkgo biloba Leaves and its Derivatives.[Reference: WebLink
This study was conducted to investigate insecticidal activities of Ginkgo biloba (L.) leaves-derived bilobalide[(-)-Bilobalide] and its hydrolysis and oxidation products against adults of Nilaparavata lugens Stal.
METHODS AND RESULTS:
To find out active insecticidal moiety of bilobalide[(-)-Bilobalide], decomposed intermediates and derivatives of bilobalide[(-)-Bilobalide] were made by hydrolysis, oxidation, and acetylation. The structures of hydrolysis product by base and oxidation product by acid were identified as cyclopentenone analogues and trilactone sesquiterpene from dehydration of bilobalide[(-)-Bilobalide], respectively. Insecticidal activities of the decomposed intermediates and the derivatives of bilobalide[(-)-Bilobalide] decreased in the order of bilobalide[(-)-Bilobalide], monoacetate, ginkgolide C, oxidation product, diacetate, and hydrolysis product.
Therefore, trilactone structure of bilobalide[(-)-Bilobalide] may be essential for its insecticidal activity.