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Purity: ≥98%
Gastrodin (Gastrodine), a brain-penetrant anti-inflammatory polyphenol extracted from Chinese natural herbal Gastrodia elata Blume, benefits neurodegenerative diseases. Gastrodin is the most important and effective ingredient extracted from Chinese natural herbal Gastrodia elata. Gastrodin (30, 40, and 60 mM) significantly attenuates levels of neurotoxic proinflammatory mediators and proinflammatory cytokines by inhibition of the NF-kappaB signaling pathway and phosphorylation of MAPKs in LPS-stimulated microglial cells.
| Targets |
Naturalproduct; ferroptosis
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| ln Vitro |
Ferroptosis is a form of necrosis caused by iron-induced accumulation of lipid hydroperoxide, involving several molecular events, and has been implicated in Parkinson's disease. Gastrodin is a component of Gastrodia elata Blume with strong antioxidant activity. We examined whether gastrodin can prevent H2O2-induced cytotoxicity in rat glioma cell line C6. For this purpose, C6 cells were pretreated with gastrodin (1, 5, 25 µM) and then exposed to 100 µM H2O2. Results showed that pretreatment of C6 cells with gastrodin decreased H2O2-induced lactate dehydrogenase (LDH) release and cell death. Moreover, gastrodin decreased intracellular malondialdehyde (MDA) level, whereas increased glutathione peroxidase (GPX) activity and glutathione (GSH) level after H2O2 treatment. In addition, treatment of deferoxamine (DFO), ferrostatin-1, and liproxstatin-1 abolished ferroptosis induced by H2O2 or erastin pretreatment. Treatment with gastrodin attenuated H2O2-induced ferroptosis and decreased lipid reactive oxygen species (ROS) (C11-BODIPY) production in C6 cells. Moreover, gastrodin increased the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), GPX4, ferroportin-1 (FPN1), and heme oxygenase-1 (HO-1) in C6 cells treated with H2O2. RSL3, a GPX4 inhibitor, inhibited GPX4 protein level in cells co-treated with gastrodin and 100 µM H2O2. These findings indicate that gastrodin can inhibit H2O2-induced ferroptosis through its antioxidative effect in C6 cells. [2]
Patients with acute ocular hypertension who receive metformin treatment have lower levels of TNF-α and iNOS mRNA expression in their retinas [1]. |
| ln Vivo |
Intraperitoneal injection of Gastrodin 10 mg/kg or 50 mg/kg once daily for 15 days effectively prevented retinal ganglion cell (RGC) loss caused by acute ocular hypertension (AOH) injury. Two weeks after AOH, the number of Iba1-positive microglia in the retina of rats injected intraperitoneally with Gastrodin1 10 mg/kg and 50 mg/kg was dramatically reduced, reaching 231.3±54.3 cells/mm2 and 201.9±43.1 cells/mm2 respectively [1].
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| Cell Assay |
Reverse Transcription-quantitative Polymerase Chain Reaction [1]
Retinas were collected at day 14 postoperatively, following treatment with NS or various doses of gastrodin. The mRNA expression levels of TNF-α and iNOS were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Total RNA was isolated using Trizol reagent and the first strand cDNA was generated by reverse transcription using one commercial reagent, according to the manufacturer's instructions. Quantitative PCR was performed using Fast Start Universal SYBR Green Master on Lightcycler 480 system. The primers used were as follows: TNF-α primers: forwad (5′-CAGGTTCCGTCCCTCTCATA-3′) and reverse (5′-TGCCAGTTCCACATCTCG-3′), iNOS primers: forwad (5′-GCAAGCCCTCACCTACTTCC-3′) and reverse (5′-AACCTCTGCCTGTGCGTCT-3′), β-actin was used as an internal control. Rat β-actin endogenous reference genes primers and the other primers were used. All reactions were performed in triplicate and average threshold cycle (Ct) values >35 were considered to be negative. The relative expression levels of mRNAs were calculated using comparative Ct method. Each group was normalized to the control group and then set at 100%. |
| Animal Protocol |
AOH rat model was performed in a randomly selected eye by anterior chamber perfusion and either received an intraperitoneal injection with various concentrations of gastrodin or normal saline. After 2wk, the rats were sacrificed. FluoroGold was used to label survival RGCs. Immunostaining with anti-Iba1 in the retinal flat mounts to calculate the microglia density in the ganglion cell layer (GCL). Changes in microglial cytokines, tumour necrosis factor-alpha (TNF-α) and inducible NO synthase (iNOS) were examined with Western blot and reverse transcription-quantitative polymerase chain reaction. Expression levels of total and phosphorylated p38 mitogen activated protein kinase (MAPK) were determined by Western blot.[1]
Adult female SD rats (age, 8wk; weight, 200-250 g) were used for all the experiments and every possible measure was performed in order to minimize animal suffering. The animals were caged individually in an environmentally controlled room (22°C-26°C) with an alternating 12h/12h light/dark cycle and enough food and water. The rats were divided into 4 groups: 1) control group; 2) normal saline (NS) group who were exposed to AOH and received intraperitoneal injection of 0.9% NS; 3) G10 group who were exposed to AOH and received intraperitoneal injection of 10 mg/kg gastrodin; 4) G50 group who were exposed to AOH and received intraperitoneal injection of 50 mg/kg gastrodin. Significant loss of RGCs is known to take place in a delayed fashion after the acute high IOP. The number of RGCs decreased to less than 50%, meanwhile, the retina microglial cells also increased significantly in number and displayed an activated morphology, as revealed by Iba1-positive cell on day 14 after acute high IOP[6]. Therefore, the loss of RGCs and the number of Iba1-positive retina microglia were determined at 2wk after rapid ocular hypertension. gastrodin), dissolved in NS, was administered intraperitoneally for 1d at the respective doses before the induction of AOH model.[1] |
| References |
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| Additional Infomation |
Gastrodin is a glycoside.
Gastrodin has been reported in Anoectochilus formosanus, Pyrus communis, and other organisms with data available. See also: Gastrodia elata tuber (part of). Many reports have indicated that gastrodin can act upon multiple pathways, such as NF-κB, ERK1/2, and iNOS, among others, except on the p38 MAPK signaling pathway. Thus, gastrodin could possibly inhibit the microglia activation dependent on different pathways, including the p38 MAPK pathway. As expected, the phosphorylation level of p38 was significantly decreased as a result of continuous gastrodin treatment. Therefore, the p38 MAPK signaling pathway is the major signaling pathway through which gastrodin exerts its anti-inflammatory effects. In addition to its anti-inflammatory effect, gastrodin can prevent the enhancement of extracellular glutamate level, which may provide extra insights to explain the neurochemical effects of gastrodin against RGCs damage induced by AOH. Further investigations are needed to elucidate the direct effect of gastrodin on cultured primary RGCs. In conclusion, we showed that gastrodin exerted its neuroprotective effects on RGCs in the AOH rat model. Gastrodin treatment significantly attenuated the production of microglia-mediated pro-inflammatory mediators, including TNF-α and iNOS. Furthermore, the level of phosphorylated p38 MAPK was significantly decreased by continuous gastrodin treatment. Taken together, these findings support our belief that the therapeutic potential of gastrodin in neuroprotective therapy for glaucoma and gastrodin can promote the survival of RGCs and may have a therapeutic potential in other degenerative optic neuropathies characterized by RGC apoptosis. [1] |
| Molecular Formula |
C13H18O7
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| Molecular Weight |
286.28
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| Exact Mass |
286.105
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| Elemental Analysis |
C, 54.54; H, 6.34; O, 39.12
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| CAS # |
62499-27-8
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| Related CAS # |
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| PubChem CID |
115067
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| Appearance |
White to off-white solid powder
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| Density |
1.5±0.1 g/cm3
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| Boiling Point |
563.2±50.0 °C at 760 mmHg
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| Melting Point |
154-157ºC
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| Flash Point |
294.4±30.1 °C
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| Vapour Pressure |
0.0±1.6 mmHg at 25°C
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| Index of Refraction |
1.638
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| LogP |
-1.85
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| Hydrogen Bond Donor Count |
5
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
20
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| Complexity |
292
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| Defined Atom Stereocenter Count |
5
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| SMILES |
C1=CC(=CC=C1CO)O[C@H]2[C@@H]([C@H]([C@@H]([C@H](O2)CO)O)O)O
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| InChi Key |
PUQSUZTXKPLAPR-UJPOAAIJSA-N
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| InChi Code |
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
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| Chemical Name |
4-(hydroxymethyl)phenyl β-D-glucopyranoside
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (8.73 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (349.31 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.4931 mL | 17.4654 mL | 34.9308 mL | |
| 5 mM | 0.6986 mL | 3.4931 mL | 6.9862 mL | |
| 10 mM | 0.3493 mL | 1.7465 mL | 3.4931 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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