Gastrodin

CAS# 62499-27-8

Gastrodin

Catalog No. BCN6306----Order now to get a substantial discount!

Product Name & Size Price Stock
Gastrodin: 5mg Please Inquire In Stock
Gastrodin: 10mg Please Inquire In Stock
Gastrodin: 20mg Please Inquire Please Inquire
Gastrodin: 50mg Please Inquire Please Inquire
Gastrodin: 100mg Please Inquire Please Inquire
Gastrodin: 200mg Please Inquire Please Inquire
Gastrodin: 500mg Please Inquire Please Inquire
Gastrodin: 1000mg Please Inquire Please Inquire

Quality Control of Gastrodin

Number of papers citing our products

Chemical structure

Gastrodin

3D structure

Chemical Properties of Gastrodin

Cas No. 62499-27-8 SDF Download SDF
PubChem ID 115067 Appearance White powder
Formula C13H18O7 M.Wt 286.28
Type of Compound Phenols Storage Desiccate at -20°C
Synonyms 4-Hydroxybenzyl alcohol 4-O-β-D-glucoside
Solubility DMSO : ≥ 100 mg/mL (349.31 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name (2R,3S,4S,5R,6S)-2-(hydroxymethyl)-6-[4-(hydroxymethyl)phenoxy]oxane-3,4,5-triol
SMILES C1=CC(=CC=C1CO)OC2C(C(C(C(O2)CO)O)O)O
Standard InChIKey PUQSUZTXKPLAPR-UJPOAAIJSA-N
Standard InChI InChI=1S/C13H18O7/c14-5-7-1-3-8(4-2-7)19-13-12(18)11(17)10(16)9(6-15)20-13/h1-4,9-18H,5-6H2/t9-,10-,11+,12-,13-/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Gastrodin

The herb of Gastrodia elata BL.

Biological Activity of Gastrodin

DescriptionGastrodin has antioxidant, cytoprotective, anticonvulsant, and anti-inflammation activities, it may be useful in the prevention and treatment of osteoporosis. Gastrodin also has protective effect to the prevention of neurotoxicity induced by ischemic stroke, the mechanism is by improving anti-oxidant and anti-inflammation activities, inhibiting apoptosis pathway, and increasing Akt phosphorylation and Nrf2 expression. Gastrodin activates PI3-K/Akt signaling and that inhibition of this pathway reverses the inhibitory effects of gastrodin on NF-κB and MAPKs activation in H9c2 cardiomyocytes.
TargetsGABA Receptor | ROS | Nrf2 | Bcl-2/Bax | HO-1 | p38MAPK | 5-HT Receptor | Caspase | Akt | TNF-α | IL Receptor | NOS | COX | PI3K | NF-kB | ERK | IkB | IKK
In vitro

Gastrodin decreases immunoreactivities of gamma-aminobutyric acid shunt enzymes in the hippocampus of seizure-sensitive gerbils.[Pubmed: 12548709 ]

J Neurosci Res. 2003 Feb 15;71(4):534-43.

Gastrodin is one of the natural compound isolated from Gastrodia elata and has known anticonvulsant effects, although the exact pharmacological principles of this natural compound and its effects on other aspects of gamma-aminobutyric acid (GABA) metabolism in vivo have not been explored.
METHODS AND RESULTS:
Therefore, in the present study, the effects of Gastrodin on GABA metabolism in the gerbil hippocampus were examined, in an effort to identify the antiepileptic characteristics of this substance. Gastrodin reduced the seizure score in the treated group, although the immunoreactivities of GABA synthetic enzymes and GABA transporters were unaltered in Gastrodin-treated animals. Interestingly, in the Gastrodin-treated group, GABA transaminase (GABA-T) immunoreactivity in the hippocampus, particularly in neurons, was significantly decreased. In the Gastrodin-treated group, both succinic semialdehyde dehydrogenase (SSADH) and succinic semialdehyde reductase (SSAR) immunoreactivities in the hippocampus was also decreased significantly, which stood in contrast to the nontreated group, in which strong SSADH and SSAR immunoreactivities were detected.
CONCLUSIONS:
From the neuroanatomical viewpoint, these findings suggest that Gastrodin may cause the elevation of GABA concentration by inhibiting the GABA shunt.

In vivo

Gastrodin: an ancient Chinese herbal medicine as a source for anti-osteoporosis agents via reducing reactive oxygen species.[Pubmed: 25554600]

Bone. 2015 Apr;73:132-44.

Increased levels of reactive oxygen species (ROS) are a crucial pathogenic factor of osteoporosis. Gastrodin, isolated from the traditional Chinese herbal agent Gastrodia elata, is a potent antioxidant. We hypothesized that Gastrodin demonstrates protective effects against osteoporosis by partially reducing reactive oxygen species in human bone marrow mesenchymal stem cells (hBMMSCs) and a macrophage cell line (RAW264.7 cells).
METHODS AND RESULTS:
We investigated Gastrodin on osteogenic and adipogenic differentiation under oxidative stress in hBMMSCs. We also tested Gastrodin on osteoclastic differentiation in RAW264.7 cells. Hydrogen peroxide (H2O2) was used to establish an oxidative cell injury model. Our results showed that Gastrodin significantly promoted the proliferation of hBMMSCs, improved some osteogenic markers, reduced lipid generation and inhibited the mRNA expression of several adipogenic genes in hBMMSCs. Moreover, Gastrodin reduced the number of osteoclasts, TRAP activity and the expression of osteoclast-specific genes in RAW264.7 cells. Gastrodin suppressed the production of reactive oxygen species in both hBMMSCs and RAW264.7 cells. In vivo, we established a murine ovariectomized (OVX) osteoporosis model. Our data revealed that Gastrodin treatment reduced the activity of serum bone degradation markers, such as CTX-1 and TRAP. Importantly, it ameliorated the micro-architecture of trabecular bones. Gastrodin decreased osteoclast numbers in vivo by TRAP staining.
CONCLUSIONS:
To conclude, these results indicated that Gastrodin shows protective effects against osteoporosis linking to a reduction in reactive oxygen species, suggesting that Gastrodin may be useful in the prevention and treatment of osteoporosis.

Gastrodin alleviates cerebral ischemic damage in mice by improving anti-oxidant and anti-inflammation activities and inhibiting apoptosis pathway.[Pubmed: 25582916 ]

Neurochem Res. 2015 Apr;40(4):661-73.

Gastrodin (GAS), an active constituent of the Chinese herbal medicine Tianma, has anti-oxidant and anti-inflammation activities but its protective effect to the prevention of neurotoxicity induced by ischemic stroke is unclear.
METHODS AND RESULTS:
In the present study, middle cerebral artery occlusion (MCAO) was used to establish a mice ischemic stroke model. Infarct volume ratio and neurobehavioral score were evaluated, Nissl staining was performed and the expression of cleaved Caspase 3, Bax and B cell lymphoma 2 (Bcl-2) were assessed at 24 h or 7 days after reperfusion. In addition, the total superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, as well as the expression of Nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), SOD1, phospho-Akt and total Akt and TNF-α and IL-1β in the ischemic hemispheres were also observed at 6 h after reperfusion to assess oxidative stress and inflammatory changes after GAS treatment. It was found that GAS, especially at high dose (100 mg/kg) reduced tested neuronal injury and neurobehavioral deficient in MCAO mice. Enhanced expression of cleaved Caspase 3 and Bax and decreased expression of Bcl-2 by MCAO were also reversed by GAS. Moreover, GAS treatment decreased the MDA content and the expression of TNF-α and IL-1β, and increased amount of SOD activity and the expression of HO-1 and SOD1 in GAS-treated ischemic brain. Furthermore, GAS significantly increased Akt phosphorylation and Nrf2 expression.
CONCLUSIONS:
These results support the neuroprotective effects of GAS, and the activation of Akt/Nrf2 pathway may play a critical role in the pharmacological action of GAS.

Protocol of Gastrodin

Kinase Assay

Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-κB and MAPKs activation via the phosphatidylinositol 3-kinase signaling.[Pubmed: 23376120 ]

Gastrodin protects against MPP(+)-induced oxidative stress by up regulates heme oxygenase-1 expression through p38 MAPK/Nrf2 pathway in human dopaminergic cells.[Pubmed: 24932697]

Neurochem Int. 2014 Sep;75:79-88.

Although the etiology of PD remains unclear, increasing evidence has shown that oxidative stress plays an important role in its pathogenesis and that of other neurodegenerative disorders. The phenolic glucoside Gastrodin, a main constituent of a Chinese herbal medicine Gastrodia elata (GE) Blume, has been known to display antioxidant activity.
METHODS AND RESULTS:
The present study aimed to investigate the protective effects of Gastrodin on 1-methyl-4-phenylpyridinium (MPP(+))-induced oxidative cytotoxicity in human dopaminergic SH-SY5Y cells and the underlying mechanism for this neuroprotection. Results indicate that pre-treatment with Gastrodin for 1h significantly reduced the MPP(+)-induced viability loss, apoptotic rate and attenuated MPP(+)-mediated ROS production. In addition, Gastrodin inhibited MPP(+)-induced lowered membrane potential, decreased Bcl-2/Bax ratio. Moreover, we have revealed the Gastrodin increased Nrf2 nuclear translocation, which is upstream of heme oxygenase-1 (HO-1) expression and for the first time revealed Gastrodin could increased antioxidant enzyme HO-1 expression in concentration-dependent and time-dependent manners. HO-1 siRNA transfection was employed, and confirmed Gastrodin could active the expression of HO-1. And the increase in HO-1 expression was correlated with the protective effect of Gastrodin against MPP(+)-induced injury. Because the inhibitor of HO-1 activity, ZnPP reversed the protective effect of Gastrodin against MPP(+)-induced cell death. We also demonstrated that the specific p38 MAPK inhibitor, SB203580, concentration-dependently blocked on Gastrodin-induced HO-1 expression, and meanwhile SB203580 reversed the protective effect of Gastrodin against MPP(+)-induced cell death.
CONCLUSIONS:
Taken together, these findings suggest that Gastrodin can induce HO-1 expression through activation of p38 MAPK/Nrf2 signaling pathway, thereby protecting the SH-SY5Y cells from MPP(+)-induced oxidative cell death. Thus our study indicates that Gastrodin has a partial cytoprotective role in dopaminergic cell culture systems and could be of importance for the treatment of PD and other oxidative stress-related diseases.

Biochem Pharmacol. 2013 Apr 15;85(8):1124-33.

The phenolic glucoside Gastrodin, a main constituent of a Chinese traditional herbal medicine, has been known to display several biological and pharmacological properties. However, the role and precise molecular mechanisms explaining how Gastrodin suppresses the inflammatory response in septic cardiac dysfunction are unknown.
METHODS AND RESULTS:
To study this, rat H9c2 cardiomyocytes were treated with Gastrodin and/or lipopolysaccharide (LPS). Our results showed that Gastrodin treatment strongly suppressed nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) family activation and upregulation of the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in LPS-stimulated H9c2 cardiomyocytes. Simultaneously, Gastrodin obviously upregulated the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling in a dose-dependent manner. However, wortmannin, a specific PI3-K inhibitor, blocked the inhibitory effects of Gastrodin on LPS-stimulated H9c2 cardiomyocytes. Furthermore, PI3-K/Akt inhibition partially abolished the inhibitory effects of Gastrodin on the phosphorylation of inhibitor κB-α (IκB-α), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK), and activity of NF-κB.
CONCLUSIONS:
Here we report activation of the PI3-K/Akt signaling by Gastrodin and that inhibition of this pathway reverses the inhibitory effects of Gastrodin on NF-κB and MAPKs activation in H9c2 cardiomyocytes.

Animal Research

Gastrodin inhibits allodynia and hyperalgesia in painful diabetic neuropathy rats by decreasing excitability of nociceptive primary sensory neurons.[Pubmed: 22761855 ]

Ameliorative effect of gastrodin on 3,3'-iminodipropionitrile-induced memory impairment in rats.[Pubmed: 25817367]

Neurosci Lett. 2015 May 6;594:40-5.

3,3'-Iminodipropionitrile (IDPN), one of the nitrile derivatives inducing neurotoxicity, causes the dyskinetic syndrome and cognitive impairment. Gastrodin is widely used to treat neurological disorders and showed to improve cognitive functions.
METHODS AND RESULTS:
The present study aimed to determine whether treatment with Gastrodin can attenuate IDPN-induced impairment of memory consolidation in the passive avoidance (PA) task, and to explore the possible neural mechanisms. Our results showed that intragastric administration of Gastrodin (200mg/kg) reversed the IDPN-induced impairment of memory consolidation as indicated by the prolonged retention latency in the PA task. Furthermore, Gastrodin reverted IDPN-induced reduction of serotonin (5-HT) and elevation of serotonin turnover ratio. Gastrodin treatment prevented the increase of serotonin transporter (SERT) and the decrease of serotonin 1A (5-HT1A) receptor expression in the hippocampus of IDPN-treated rats.
CONCLUSIONS:
These results suggest that long-term Gastrodin treatment could represent a novel pharmacological strategy for IDPN-induced memory impairment, as well that its protective effect is mediated through normalization of the serotoninergic system.

PLoS One. 2012;7(6):e39647.

Painful diabetic neuropathy (PDN) is a common complication of diabetes mellitus and adversely affects the patients' quality of life. Evidence has accumulated that PDN is associated with hyperexcitability of peripheral nociceptive primary sensory neurons. However, the precise cellular mechanism underlying PDN remains elusive. This may result in the lacking of effective therapies for the treatment of PDN. The phenolic glucoside, Gastrodin, which is a main constituent of the Chinese herbal medicine Gastrodia elata Blume, has been widely used as an anticonvulsant, sedative, and analgesic since ancient times. However, the cellular mechanisms underlying its analgesic actions are not well understood.
METHODS AND RESULTS:
By utilizing a combination of behavioral surveys and electrophysiological recordings, the present study investigated the role of Gastrodin in an experimental rat model of STZ-induced PDN and to further explore the underlying cellular mechanisms. Intraperitoneal administration of Gastrodin effectively attenuated both the mechanical allodynia and thermal hyperalgesia induced by STZ injection. Whole-cell patch clamp recordings were obtained from nociceptive, capsaicin-sensitive small diameter neurons of the intact dorsal root ganglion (DRG). Recordings from diabetic rats revealed that the abnormal hyperexcitability of neurons was greatly abolished by application of GAS. To determine which currents were involved in the antinociceptive action of Gastrodin, we examined the effects of Gastrodin on transient sodium currents (I(NaT)) and potassium currents in diabetic small DRG neurons. Diabetes caused a prominent enhancement of I(NaT) and a decrease of potassium currents, especially slowly inactivating potassium currents (I(AS)); these effects were completely reversed by GAS in a dose-dependent manner. Furthermore, changes in activation and inactivation kinetics of I(NaT) and total potassium current as well as I(AS) currents induced by STZ were normalized by GAS.
CONCLUSIONS:
This study provides a clear cellular basis for the peripheral analgesic action of Gastrodin for the treatment of chronic pain, including PDN.

Gastrodin Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Gastrodin Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Gastrodin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.4931 mL 17.4654 mL 34.9308 mL 69.8617 mL 87.3271 mL
5 mM 0.6986 mL 3.4931 mL 6.9862 mL 13.9723 mL 17.4654 mL
10 mM 0.3493 mL 1.7465 mL 3.4931 mL 6.9862 mL 8.7327 mL
50 mM 0.0699 mL 0.3493 mL 0.6986 mL 1.3972 mL 1.7465 mL
100 mM 0.0349 mL 0.1747 mL 0.3493 mL 0.6986 mL 0.8733 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Gastrodin

Gastrodin protects against MPP(+)-induced oxidative stress by up regulates heme oxygenase-1 expression through p38 MAPK/Nrf2 pathway in human dopaminergic cells.[Pubmed:24932697]

Neurochem Int. 2014 Sep;75:79-88.

Although the etiology of PD remains unclear, increasing evidence has shown that oxidative stress plays an important role in its pathogenesis and that of other neurodegenerative disorders. The phenolic glucoside Gastrodin, a main constituent of a Chinese herbal medicine Gastrodia elata (GE) Blume, has been known to display antioxidant activity. The present study aimed to investigate the protective effects of Gastrodin on 1-methyl-4-phenylpyridinium (MPP(+))-induced oxidative cytotoxicity in human dopaminergic SH-SY5Y cells and the underlying mechanism for this neuroprotection. Results indicate that pre-treatment with Gastrodin for 1h significantly reduced the MPP(+)-induced viability loss, apoptotic rate and attenuated MPP(+)-mediated ROS production. In addition, Gastrodin inhibited MPP(+)-induced lowered membrane potential, decreased Bcl-2/Bax ratio. Moreover, we have revealed the Gastrodin increased Nrf2 nuclear translocation, which is upstream of heme oxygenase-1 (HO-1) expression and for the first time revealed Gastrodin could increased antioxidant enzyme HO-1 expression in concentration-dependent and time-dependent manners. HO-1 siRNA transfection was employed, and confirmed Gastrodin could active the expression of HO-1. And the increase in HO-1 expression was correlated with the protective effect of Gastrodin against MPP(+)-induced injury. Because the inhibitor of HO-1 activity, ZnPP reversed the protective effect of Gastrodin against MPP(+)-induced cell death. We also demonstrated that the specific p38 MAPK inhibitor, SB203580, concentration-dependently blocked on Gastrodin-induced HO-1 expression, and meanwhile SB203580 reversed the protective effect of Gastrodin against MPP(+)-induced cell death. Taken together, these findings suggest that Gastrodin can induce HO-1 expression through activation of p38 MAPK/Nrf2 signaling pathway, thereby protecting the SH-SY5Y cells from MPP(+)-induced oxidative cell death. Thus our study indicates that Gastrodin has a partial cytoprotective role in dopaminergic cell culture systems and could be of importance for the treatment of PD and other oxidative stress-related diseases.

Gastrodin inhibits allodynia and hyperalgesia in painful diabetic neuropathy rats by decreasing excitability of nociceptive primary sensory neurons.[Pubmed:22761855]

PLoS One. 2012;7(6):e39647.

Painful diabetic neuropathy (PDN) is a common complication of diabetes mellitus and adversely affects the patients' quality of life. Evidence has accumulated that PDN is associated with hyperexcitability of peripheral nociceptive primary sensory neurons. However, the precise cellular mechanism underlying PDN remains elusive. This may result in the lacking of effective therapies for the treatment of PDN. The phenolic glucoside, Gastrodin, which is a main constituent of the Chinese herbal medicine Gastrodia elata Blume, has been widely used as an anticonvulsant, sedative, and analgesic since ancient times. However, the cellular mechanisms underlying its analgesic actions are not well understood. By utilizing a combination of behavioral surveys and electrophysiological recordings, the present study investigated the role of Gastrodin in an experimental rat model of STZ-induced PDN and to further explore the underlying cellular mechanisms. Intraperitoneal administration of Gastrodin effectively attenuated both the mechanical allodynia and thermal hyperalgesia induced by STZ injection. Whole-cell patch clamp recordings were obtained from nociceptive, capsaicin-sensitive small diameter neurons of the intact dorsal root ganglion (DRG). Recordings from diabetic rats revealed that the abnormal hyperexcitability of neurons was greatly abolished by application of GAS. To determine which currents were involved in the antinociceptive action of Gastrodin, we examined the effects of Gastrodin on transient sodium currents (I(NaT)) and potassium currents in diabetic small DRG neurons. Diabetes caused a prominent enhancement of I(NaT) and a decrease of potassium currents, especially slowly inactivating potassium currents (I(AS)); these effects were completely reversed by GAS in a dose-dependent manner. Furthermore, changes in activation and inactivation kinetics of I(NaT) and total potassium current as well as I(AS) currents induced by STZ were normalized by GAS. This study provides a clear cellular basis for the peripheral analgesic action of Gastrodin for the treatment of chronic pain, including PDN.

Gastrodin: an ancient Chinese herbal medicine as a source for anti-osteoporosis agents via reducing reactive oxygen species.[Pubmed:25554600]

Bone. 2015 Apr;73:132-44.

Increased levels of reactive oxygen species (ROS) are a crucial pathogenic factor of osteoporosis. Gastrodin, isolated from the traditional Chinese herbal agent Gastrodia elata, is a potent antioxidant. We hypothesized that Gastrodin demonstrates protective effects against osteoporosis by partially reducing reactive oxygen species in human bone marrow mesenchymal stem cells (hBMMSCs) and a macrophage cell line (RAW264.7 cells). We investigated Gastrodin on osteogenic and adipogenic differentiation under oxidative stress in hBMMSCs. We also tested Gastrodin on osteoclastic differentiation in RAW264.7 cells. Hydrogen peroxide (H2O2) was used to establish an oxidative cell injury model. Our results showed that Gastrodin significantly promoted the proliferation of hBMMSCs, improved some osteogenic markers, reduced lipid generation and inhibited the mRNA expression of several adipogenic genes in hBMMSCs. Moreover, Gastrodin reduced the number of osteoclasts, TRAP activity and the expression of osteoclast-specific genes in RAW264.7 cells. Gastrodin suppressed the production of reactive oxygen species in both hBMMSCs and RAW264.7 cells. In vivo, we established a murine ovariectomized (OVX) osteoporosis model. Our data revealed that Gastrodin treatment reduced the activity of serum bone degradation markers, such as CTX-1 and TRAP. Importantly, it ameliorated the micro-architecture of trabecular bones. Gastrodin decreased osteoclast numbers in vivo by TRAP staining. To conclude, these results indicated that Gastrodin shows protective effects against osteoporosis linking to a reduction in reactive oxygen species, suggesting that Gastrodin may be useful in the prevention and treatment of osteoporosis.

Ameliorative effect of gastrodin on 3,3'-iminodipropionitrile-induced memory impairment in rats.[Pubmed:25817367]

Neurosci Lett. 2015 May 6;594:40-5.

3,3'-Iminodipropionitrile (IDPN), one of the nitrile derivatives inducing neurotoxicity, causes the dyskinetic syndrome and cognitive impairment. Gastrodin is widely used to treat neurological disorders and showed to improve cognitive functions. The present study aimed to determine whether treatment with Gastrodin can attenuate IDPN-induced impairment of memory consolidation in the passive avoidance (PA) task, and to explore the possible neural mechanisms. Our results showed that intragastric administration of Gastrodin (200mg/kg) reversed the IDPN-induced impairment of memory consolidation as indicated by the prolonged retention latency in the PA task. Furthermore, Gastrodin reverted IDPN-induced reduction of serotonin (5-HT) and elevation of serotonin turnover ratio. Gastrodin treatment prevented the increase of serotonin transporter (SERT) and the decrease of serotonin 1A (5-HT1A) receptor expression in the hippocampus of IDPN-treated rats. These results suggest that long-term Gastrodin treatment could represent a novel pharmacological strategy for IDPN-induced memory impairment, as well that its protective effect is mediated through normalization of the serotoninergic system.

Gastrodin decreases immunoreactivities of gamma-aminobutyric acid shunt enzymes in the hippocampus of seizure-sensitive gerbils.[Pubmed:12548709]

J Neurosci Res. 2003 Feb 15;71(4):534-43.

Gastrodin is one of the natural compound isolated from Gastrodia elata and has known anticonvulsant effects, although the exact pharmacological principles of this natural compound and its effects on other aspects of gamma-aminobutyric acid (GABA) metabolism in vivo have not been explored. Therefore, in the present study, the effects of Gastrodin on GABA metabolism in the gerbil hippocampus were examined, in an effort to identify the antiepileptic characteristics of this substance. Gastrodin reduced the seizure score in the treated group, although the immunoreactivities of GABA synthetic enzymes and GABA transporters were unaltered in Gastrodin-treated animals. Interestingly, in the Gastrodin-treated group, GABA transaminase (GABA-T) immunoreactivity in the hippocampus, particularly in neurons, was significantly decreased. In the Gastrodin-treated group, both succinic semialdehyde dehydrogenase (SSADH) and succinic semialdehyde reductase (SSAR) immunoreactivities in the hippocampus was also decreased significantly, which stood in contrast to the nontreated group, in which strong SSADH and SSAR immunoreactivities were detected. From the neuroanatomical viewpoint, these findings suggest that Gastrodin may cause the elevation of GABA concentration by inhibiting the GABA shunt.

Gastrodin attenuation of the inflammatory response in H9c2 cardiomyocytes involves inhibition of NF-kappaB and MAPKs activation via the phosphatidylinositol 3-kinase signaling.[Pubmed:23376120]

Biochem Pharmacol. 2013 Apr 15;85(8):1124-33.

The phenolic glucoside Gastrodin, a main constituent of a Chinese traditional herbal medicine, has been known to display several biological and pharmacological properties. However, the role and precise molecular mechanisms explaining how Gastrodin suppresses the inflammatory response in septic cardiac dysfunction are unknown. To study this, rat H9c2 cardiomyocytes were treated with Gastrodin and/or lipopolysaccharide (LPS). Our results showed that Gastrodin treatment strongly suppressed nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinases (MAPKs) family activation and upregulation of the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) in LPS-stimulated H9c2 cardiomyocytes. Simultaneously, Gastrodin obviously upregulated the phosphatidylinositol 3-kinase (PI3-K)/Akt signaling in a dose-dependent manner. However, wortmannin, a specific PI3-K inhibitor, blocked the inhibitory effects of Gastrodin on LPS-stimulated H9c2 cardiomyocytes. Furthermore, PI3-K/Akt inhibition partially abolished the inhibitory effects of Gastrodin on the phosphorylation of inhibitor kappaB-alpha (IkappaB-alpha), extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK), and activity of NF-kappaB. Here we report activation of the PI3-K/Akt signaling by Gastrodin and that inhibition of this pathway reverses the inhibitory effects of Gastrodin on NF-kappaB and MAPKs activation in H9c2 cardiomyocytes.

Gastrodin alleviates cerebral ischemic damage in mice by improving anti-oxidant and anti-inflammation activities and inhibiting apoptosis pathway.[Pubmed:25582916]

Neurochem Res. 2015 Apr;40(4):661-73.

Gastrodin (GAS), an active constituent of the Chinese herbal medicine Tianma, has anti-oxidant and anti-inflammation activities but its protective effect to the prevention of neurotoxicity induced by ischemic stroke is unclear. In the present study, middle cerebral artery occlusion (MCAO) was used to establish a mice ischemic stroke model. Infarct volume ratio and neurobehavioral score were evaluated, Nissl staining was performed and the expression of cleaved Caspase 3, Bax and B cell lymphoma 2 (Bcl-2) were assessed at 24 h or 7 days after reperfusion. In addition, the total superoxide dismutase (SOD) activity and malondialdehyde (MDA) content, as well as the expression of Nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), SOD1, phospho-Akt and total Akt and TNF-alpha and IL-1beta in the ischemic hemispheres were also observed at 6 h after reperfusion to assess oxidative stress and inflammatory changes after GAS treatment. It was found that GAS, especially at high dose (100 mg/kg) reduced tested neuronal injury and neurobehavioral deficient in MCAO mice. Enhanced expression of cleaved Caspase 3 and Bax and decreased expression of Bcl-2 by MCAO were also reversed by GAS. Moreover, GAS treatment decreased the MDA content and the expression of TNF-alpha and IL-1beta, and increased amount of SOD activity and the expression of HO-1 and SOD1 in GAS-treated ischemic brain. Furthermore, GAS significantly increased Akt phosphorylation and Nrf2 expression. These results support the neuroprotective effects of GAS, and the activation of Akt/Nrf2 pathway may play a critical role in the pharmacological action of GAS.

Description

Gastrodin, a main constituent of a Chinese herbal medicine Tianma, has been known to display anti-inflammatory effects. Gastrodin, has long been used for treating dizziness, epilepsy, stroke and dementia.

Keywords:

Gastrodin,62499-27-8,4-Hydroxybenzyl alcohol 4-O-β-D-glucoside,Natural Products, buy Gastrodin , Gastrodin supplier , purchase Gastrodin , Gastrodin cost , Gastrodin manufacturer , order Gastrodin , high purity Gastrodin

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: