1. Apoptosis Autophagy Metabolic Enzyme/Protease Immunology/Inflammation NF-κB PI3K/Akt/mTOR MAPK/ERK Pathway Stem Cell/Wnt
  2. Bcl-2 Family Caspase Apoptosis Autophagy Reactive Oxygen Species (ROS) Akt JNK ERK
  3. Ginkgo biloba extract

Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves. Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy). Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis.

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Ginkgo biloba extract

Ginkgo biloba extract Chemical Structure

CAS No. : 90045-36-6

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Description

Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves. Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy). Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis[1][2].

In Vitro

Ginkgo biloba extract (15 μg; 24 h) alleviates Deltamethrin (HY-B1971)-induced autophagy, abnormal ubiquitination function, blood-testis barrier (BTB) disruption, and cellular structural damage in mouse TM4 Sertoli cells by upregulating SKP2 expression and downregulating Beclin1 expression[2].
Ginkgo biloba extract attenuates hydrogen peroxide/FeSO4-induced oxidative damage in cultured rat cerebellar granule cells in vitro[3].
Ginkgo biloba extract significantly reduces basal and inducible hydrogen peroxide-related reactive oxygen species levels in Aβ-expressing mouse neuroblastoma N2a cells[3].
Ginkgo biloba extract protects cultured neurons in vitro against death induced by a variety of toxic stimuli, including hydrogen peroxide (H2O2), hypoxia, glutamate, Verapamil (HY-14275), β-amyloid, MPTP (HY-W114750), NO, and cyanide[3].
Ginkgo biloba extract attenuates oxidative stress-induced neuronal apoptosis by stabilizing mitochondrial function, regulating Bcl-2 family proteins, and inhibiting caspase activation[3].
Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, reactive oxygen species (ROS) accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Ginkgo biloba extract (100 mg/kg; p.o.; daily; 30 days) alleviates Deltamethrin-induced testicular injury in male ICR mice by upregulating SKP2, inhibiting Beclin1-independent autophagy, restoring blood-testis barrier integrity, and improving spermatogenic function and hormone levels[2].
Ginkgo biloba extract (EGb761) (10-100 mg/kg; p.o.; i.p.) reduces neuronal damage in rats and gerbils with ischemic stroke[3].
Ginkgo biloba extract (10-100 mg/kg; p.o.; i.p.) attenuates hypoxia-, heat stress- and subchronic cold stress-induced neuronal damage in rats[3].
Ginkgo biloba extract (10-100 mg/kg; p.o.; i.p.) reduces amphetamine-induced behavioral sensitization in rats[3].
Ginkgo biloba extract (10-100 mg/kg; p.o.; i.p.) alleviates neuronal damage in transgenic mouse models of amyotrophic lateral sclerosis[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: ICR mice (3-week-old male)[2]
Dosage: 100 mg/kg (co-administered with 10 mg/kg deltamethrin in combination group)
Administration: p.o.; daily; 30 days
Result: Restored daily food intake to control levels, alleviated testicular congestion and atrophy, and restored testicular index and anogenital distance to control levels compared to deltamethrin-only treated mice.
Increased serum testosterone and inhibin B levels compared to deltamethrin-only treated mice.
Improved seminiferous tubule integrity, reduced vacuolization, restored orderly arrangement of germ cells, increased presence of elongated spermatocytes, and improved Johnsen score with no germ cell detachment in tubule lumens compared to deltamethrin-only treated mice.
Preserved sperm structural integrity, attenuated cellular autophagy, and reduced mitochondrial vacuolization compared to deltamethrin-only treated mice.
Significantly increased gene expression levels of spermatogenesis-related factors TNP1, TNP2, PRM1, and PRM2, and significantly decreased protein levels of histones H2B and H3 compared to deltamethrin-only treated mice.
Increased protein expression levels of Claudin1, Occludin, and β-catenin to restore blood-testis barrier integrity compared to deltamethrin-only treated mice.
Decreased testicular mRNA expression levels of Atg5, Atg12, Atg7, LC3B, and Beclin1, increased mRNA expression of mTOR and P62, decreased protein expression levels of LC3B II/LC3B I and Beclin1, and increased P62 protein expression to inhibit autophagy compared to deltamethrin-only treated mice.
Increased testicular mRNA and protein expression levels of SKP2, Ring1b, and RNF8, and restored serum levels of E3 ubiquitin ligase and deubiquitinases to improve ubiquitination function compared to deltamethrin-only treated mice.
Animal Model: unspecified strain[3]
Dosage: 10 mg/kg; 100 mg/kg
Administration: p.o.; i.p.
Result: Reduced neuronal damage.
Animal Model: hypoxia/Heat stress/Subchronic cold stress-induced rat[3]
Dosage: 10 mg/kg; 100 mg/kg
Administration: p.o.; i.p.
Result: Reduced neuronal damage.
Animal Model: Rat[3]
Dosage: 10 mg/kg; 100 mg/kg
Administration: p.o.; i.p.
Result: Reduced amphetamine-induced behavioral sensitization.
Animal Model: transgenic strain (amyotrophic lateral sclerosis model)[3]
Dosage: 10 mg/kg; 100 mg/kg
Administration: p.o.; i.p.
Result: Reduced neuronal damage.
CAS No.
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Solid

Color

Light brown to brown

SMILES

[Ginkgo biloba extract]

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Room temperature in continental US; may vary elsewhere.

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4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

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DMSO : 2.5 mg/mL (ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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