Enhanced bioaccessibility in vitro and bioavailability of Ginkgo biloba extract nanoparticles prepared by liquid anti‐solvent precipitation

2019 ◽  
Vol 54 (6) ◽  
pp. 2266-2276 ◽  
Author(s):  
Lingling Wang ◽  
Xiuhua Zhao ◽  
Fengjian Yang ◽  
Weiwei Wu ◽  
Yanjie Liu ◽  
...  
Keyword(s):  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract

Effect of Ginkgo biloba extract on rat hepatic microsomal CYP1A activity: role of ginkgolides, bilobalide, and flavonols

2004 ◽  
Vol 82 (1) ◽  
pp. 57-64 ◽  
Author(s):  
I fan Kuo ◽  
Jie Chen ◽  
Thomas K.H Chang
Keyword(s):  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Inhibitory Potency ◽  
Hepatic Microsomes ◽  
Cyp1a Activity ◽  
Ginkgo Biloba Extracts ◽  
The Individual ◽  
Vitro Effect

The present study investigated the in vitro effect of Ginkgo biloba extracts and some of the individual constituents (ginkgolides, bilobalide, and flavonols such as kaempferol, quercetin, isorhamnetin, and their glycosides) on CYP1A-mediated 7-ethoxyresorufin O-dealkylation in hepatic microsomes isolated from rats induced with β-naphthoflavone. G. biloba extract competitively inhibited CYP1A activity, with an apparent Ki value of 1.6 ± 0.4 µg/mL (mean ± SE). At the concentrations present in the G. biloba extracts, ginkgolides A, B, C, and J and bilobalide did not affect CYP1A activity, whereas kaempferol (IC50 = 0.006 ± 0.001 µg/mL, mean ± SE), isorhamnetin (0.007 ± 0.001 µg/mL), and quercetin (0.050 ± 0.003 µg/mL) decreased this activity. The monoglycosides (1 and 10 µg/mL) and diglycosides (10 µg/mL) of kaempferol and quercetin but not those of isorhamnetin also inhibited CYP1A activity. The order of inhibitory potency was kaempferol ~ isorhamnetin > quercetin, and for each of these flavonols the order of potency was aglycone >> monoglycoside > diglycoside. In summary, G. biloba extract competitively inhibited rat hepatic microsomal CYP1A activity, but the effect was not due to ginkgolides A, B, C, or J, bilobalide, kaempferol, quercetin, isorhamnetin, or the respective flavonol monoglycosides or diglycosides.Key words: bilobalide, CYP1A, cytochrome P450, Ginkgo biloba, ginkgolide, flavonol.

scholarly journals ANTIOXIDANT, CYTOTOXICITY, AND STABILITY EVALUATION OF GINKGO BILOBA EXTRACT-BASED MICROEMULSIONS FOR ENHANCED THERAPEUTIC ACTIVITY

2017 ◽  
Vol 10 (8) ◽  
pp. 335 ◽  
Author(s):  
Manisha Singh ◽  
Surya Pratap Singh ◽  
Rachana R
Keyword(s):  
Ginkgo Biloba ◽  
Therapeutic Potential ◽  
Ginkgo Biloba Extract ◽  
In Vitro Cytotoxicity ◽  
Scavenging Activity ◽  
Therapeutic Implications ◽  
Chromatography Analysis ◽  
Ic50 Value ◽  
Cytotoxicity Assessment

Objective: This study is aimed to evaluate the antioxidant (AO) potential, cytotoxicity, and stability of preformulated Ginkgo biloba standard extractmicroemulsion (GBME), to investigate if, it retains the therapeutic potential of EGB761 and remains safe and stable for a longer period.Method and Results: GBME has shown enhanced AO (85.2±0.78%, IC50=31.3±0.45 μg/ml) in comparison to EGB761 (74.1±0.51%,IC50=49.4±0.05 μg/ml) using 2,2’-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) assay. Similarly, 2,2-diphenyl-1-picryl-hydrazyl-hydrate(DPPH) assay has also shown that AO for GBME (94.6±0.04%, IC50=11.4±1.03 μg/ml) was higher than EGB761 (78.6±1.20%, IC50=34.6±0.81 μg/ml).Further, IC50 value of antiradical unit of GBME was much lesser (ABTS=14.3±1.05 μg/ml and DPPH=17.03±1.8 μg/ml) in comparison to EGB761(ABTS=34.1±1.62 μg/ml and DPPH=37.5±0.08 μg/ml). Equivalently, both, hydrogen peroxide scavenging activity, and nitric oxide activity wereappreciably higher for GBME than the pure extract. The in vitro cytotoxicity assessment showed that GBME is quite safe (98.68±0.76% cell viability) incomparison to EGB761 (83.29±1.02%). Thereafter, these samples were tested for stability by evaluating their AO activity along with high-performanceliquid chromatography analysis, for the major phytocompounds, after 1 year, and results suggested that AO of GBME remained stable while comparingwith the freshly prepared GBME, whereas AO of EGB761 reduced significantly as compared to freshly taken EGB761 extract implying the degradationof phytocompounds supporting decrease in AO activity.Conclusion: Therefore, the observed results suggest that GBME maintained AO and scavenging activity along with enhanced shelf life with no observedtoxicity, which can be explored further for its potential therapeutic implications in various oxidative stress-induced central nervous system disorders.

Effects of Ginkgo biloba Extract Ingestion on the Pharmacokinetics of Talinolol in Healthy Chinese Volunteers

2009 ◽  
Vol 43 (5) ◽  
pp. 944-949 ◽  
Author(s):  
Lan Fan ◽  
Gong-You Tao ◽  
Guo Wang ◽  
Yao Chen ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Oral Dose ◽  
Single Oral Dose ◽  
Ginkgo Biloba ◽  
High Performance ◽  
Plasma Concentrations ◽  
Ginkgo Biloba Extract ◽  
Maximum Plasma ◽  
Time Curve ◽  
P Glycoprotein

Background Ginkgo biloba extract (GBE), the best selling herbal medicine in the world, has been reported to inhibit P-glycoprotein in vitro. However, the effects of GBE on P-glycoprotein activity in humans have not been clarified. Objective To investigate the effects of single and repeated GBE ingestion on the oral pharmacokinetics of talinolol, a substrate drug for P-glycoprotein in humans. Methods Ten unrelated healthy male volunteers were selected to participate in a 3-stage sequential study. Plasma concentrations of talinolol from 0 to 24 hours were measured by high-performance liquid chromatography after talinolol 100 mg was administrated alone, with a single oral dose of GBE (120 mg), and after 14 days of repeated GBE ingestion (360 mg/day). Results A single oral dose of GBE did not affect the pharmacokinetics of talinolol. Repeated ingestion of GBE increased the talinolol maximum plasma concentration (Cmax) by 36% (90% CI 10 to 68; p = 0.025), the area under the concentration-time curve (AUC)0-24 by 26% (90% CI 11 to 43; p = 0.008) and AUC0-∞ by 22% (90% CI 8 to 37; p = 0.014), respectively, without significant changes in elimination half-life and the time to Cmax. Conclusions Our results suggest that long-term use of GBE significantly influenced talinolol disposition in humans, likely by affecting the activity of P-glycoprotein and/or other drug transporters.

scholarly journals EGb761, a Ginkgo Biloba Extract, Is Effective Against Atherosclerosis In Vitro, and in a Rat Model of Type 2 Diabetes

PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e20301 ◽  
Author(s):  
Soo Lim ◽  
Ji Won Yoon ◽  
Seon Mee Kang ◽  
Sung Hee Choi ◽  
Bong Jun Cho ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Rat Model ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract

Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells

2009 ◽  
Vol 106 (5) ◽  
pp. 1674-1685 ◽  
Author(s):  
Hsiu-Chung Ou ◽  
Wen-Jane Lee ◽  
I-Te Lee ◽  
Tsan-Hung Chiu ◽  
Kun-Ling Tsai ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ginkgo Biloba ◽  
Umbilical Vein ◽  
Density Lipoprotein ◽  
Ginkgo Biloba Extract ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Vascular Endothelial ◽  
Cytochrome C Release

Atherosclerosis is a chronic inflammatory process with increased oxidative stress in vascular endothelium. Ginkgo biloba extract (GbE), extracted from Ginkgo biloba leaves, has commonly been used as a therapeutic agent for cardiovascular and neurological disorders. The aim of this study was to investigate how GbE protects vascular endothelial cells against the proatherosclerotic stressor oxidized low-density lipoprotein (oxLDL) in vitro. Human umbilical vein endothelial cells (HUVECs) were incubated with GbE (12.5–100 μg/ml) for 2 h and then incubated with oxLDL (150 μg/ml) for an additional 24 h. Subsequently, reactive oxygen species (ROS) generation, antioxidant enzyme activities, adhesion to monocytes, cell morphology, viability, and several apoptotic indexes were assessed. Our data show that ROS generation is an upstream signal in oxLDL-treated HUVECs. Cu,Zn-SOD, but not Mn-SOD, was inactivated by oxLDL. In addition, oxLDL diminished expression of endothelial NO synthase and enhanced expression of adhesion molecules (ICAM, VCAM, and E-selectin) and the adherence of monocytic THP-1 cells to HUVECs. Furthermore, oxLDL increased intracellular calcium, disturbed the balance of Bcl-2 family proteins, destabilized mitochondrial membrane potential, and triggered subsequent cytochrome c release into the cytosol and activation of caspase-3. These detrimental effects were ameliorated dose dependently by GbE ( P < 0.05). Results from this study may provide insight into a possible molecular mechanism underlying GbE suppression of the oxLDL-mediated vascular endothelial dysfunction.

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