| Size | Price | Stock | Qty |
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| 10mg |
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| 25mg |
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| 100mg |
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| Targets |
- Calycosin-7-O-β-D-glucoside targets the nitric oxide (NO)/caveolin-1 (Cav-1)/matrix metalloproteinases (MMPs) pathway [1]
- Calycosin-7-O-β-D-glucoside targets the SIRT1/FOXO1/PGC-1α pathway [2] |
|---|---|
| ln Vitro |
In microvessels isolated from ischemic rat brain, calycosin-7-O-β-D-glucoside (2 μM; 6 h) strongly suppresses MMPs' expression and activity while ensuring the expression of tight junction proteins and cav-1 [1].
- In HT22 hippocampal neuronal cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury (12 h OGD + 24 h reoxygenation), Calycosin-7-O-β-D-glucoside (10, 20, 40 μM) exerted dose-dependent protective effects: (1) Enhanced cell viability (detected by CCK-8 assay), with the 40 μM dose increasing viability by ~35% compared to the OGD/R group. (2) Reduced oxidative stress: Decreased intracellular reactive oxygen species (ROS) accumulation (DCFH-DA staining) and malondialdehyde (MDA) levels, while increased superoxide dismutase (SOD) and glutathione (GSH) activities. (3) Inhibited neuronal apoptosis: Decreased TUNEL-positive cell rate (by ~40% at 40 μM) and caspase-3/9 activities; downregulated Bax protein expression and upregulated Bcl-2 expression (Western blot). (4) Activated the SIRT1/FOXO1/PGC-1α pathway: Increased SIRT1, PGC-1α protein expression and FOXO1 deacetylation; these effects were abolished by the SIRT1 inhibitor EX527 (10 μM), confirming pathway dependence. (5) Upregulated mRNA levels of SIRT1, FOXO1, PGC-1α, and Bcl-2, and downregulated Bax mRNA (qRT-PCR) [2] |
| ln Vivo |
In an in vivo MCAO ischemia-reperfusion rat model of barrier permeability, verbascoside-7-O-β-D-glucoside (ip; 26.8 mg/kg; 14 days) dramatically lowers infarct volume, histological damage, and blood brain [1].
- In Sprague-Dawley rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury (2 h occlusion + 24 h reperfusion), Calycosin-7-O-β-D-glucoside (5, 10, 20 mg/kg, i.p.) administered 30 minutes before reperfusion showed dose-dependent neuroprotective effects: (1) Improved neurological function: Reduced modified neurological severity score (mNSS) by ~30-50% compared to the MCAO/R group, with the 20 mg/kg dose most effective. (2) Reduced cerebral infarction volume (TTC staining) by ~25-45% in a dose-dependent manner. (3) Protected blood-brain barrier (BBB) integrity: Decreased Evans blue (EB) extravasation (by ~30-50%) and increased BBB tight junction protein (ZO-1, occludin) expression (Western blot and immunohistochemistry). (4) Regulated the NO/Cav-1/MMPs pathway: Decreased nitric oxide synthase (iNOS) activity and NO production; upregulated Cav-1 protein expression; downregulated MMP-2 and MMP-9 protein expression and activity (gelatin zymography). (5) Attenuated brain tissue oxidative stress: Decreased MDA levels and increased SOD activity [1] |
| Enzyme Assay |
- SIRT1 activity assay: HT22 cells were treated with Calycosin-7-O-β-D-glucoside (10-40 μM) for 24 h, with or without EX527 (10 μM). Cell lysates were prepared, and SIRT1 activity was measured using a specific assay kit, which detects the deacetylation of a fluorescent substrate. The relative activity was calculated by comparing fluorescence intensity to the control group [2]
- MMP-2/MMP-9 activity assay (gelatin zymography): Brain tissue homogenates from MCAO/R rats were prepared, and proteins were separated by SDS-PAGE containing gelatin. After renaturation and incubation, the gel was stained with Coomassie brilliant blue and destained. Clear bands corresponding to MMP-2 and MMP-9 activity were quantified by image analysis software, with activity expressed as relative density compared to the MCAO/R group [1] - NO production and iNOS activity assay: Brain tissue homogenates were mixed with Griess reagent to detect NO production by measuring absorbance at 540 nm. iNOS activity was determined using an assay kit that measures the conversion of L-arginine to L-citrulline, with activity calculated based on standard curves [1] |
| Cell Assay |
- OGD/R-induced HT22 cell injury assay: HT22 cells were seeded in culture plates and divided into control, OGD/R, and Calycosin-7-O-β-D-glucoside (10, 20, 40 μM) groups, with an additional EX527 (10 μM) intervention group. OGD was induced by incubating cells in glucose-free medium in a hypoxic chamber (95% N₂ + 5% CO₂) for 12 h, followed by reoxygenation in normal medium for 24 h. (1) Cell viability was detected by CCK-8 assay after reoxygenation. (2) ROS accumulation was measured by DCFH-DA staining and flow cytometry. (3) Apoptosis was assessed by TUNEL staining (immunofluorescence) and annexin V-FITC/PI double staining (flow cytometry); caspase-3/9 activities were detected by colorimetric assay kits. (4) Western blot was performed to detect SIRT1, acetyl-FOXO1, FOXO1, PGC-1α, Bax, Bcl-2 protein expression. (5) Total RNA was isolated for qRT-PCR to quantify SIRT1, FOXO1, PGC-1α, Bax, Bcl-2 mRNA levels [2]
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| Animal Protocol |
Animal/Disease Models: Middle cerebral artery occlusion (MCAO) male adult Sprague-Daweley rat [1]
Doses: 26.8 mg/kg Route of Administration: intraperitoneal (ip) injection; 26.8 mg/kg; 14 days Experimental Results: Neuroprotective effect on rats . - MCAO/R injury model in Sprague-Dawley rats: Male Sprague-Dawley rats were randomly divided into sham, MCAO/R, and Calycosin-7-O-β-D-glucoside (5, 10, 20 mg/kg) groups (n=10 per group). (1) Model preparation: MCAO was induced by inserting a nylon suture into the right middle cerebral artery for 2 h, then reperfused by removing the suture. Sham-operated rats underwent the same procedure without suture insertion. (2) Drug administration: Calycosin-7-O-β-D-glucoside was dissolved in normal saline and administered intraperitoneally 30 minutes before reperfusion; the sham and MCAO/R groups received equal volumes of normal saline. (3) Neurological function assessment: mNSS was evaluated 24 h after reperfusion. (4) Sample collection: Rats were euthanized, and brains were harvested for TTC staining (infarction volume), EB extravasation assay (BBB integrity), Western blot (ZO-1, occludin, Cav-1, MMP-2, MMP-9), immunohistochemistry (Cav-1, MMP-9), and oxidative stress index (SOD, MDA) detection [1] |
| References |
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| Additional Infomation |
Mangosteen-7-O-β-D-glucoside is a glycosyl isoflavone formed by the substitution of mangosteen at the 7-position by a glycosidic bond with a β-D-glucopyranose residue. It is a hydroxy isoflavone, a monosaccharide derivative, belonging to the 4'-methoxy isoflavone and 7-hydroxy isoflavone 7-O-β-D-glucoside class of compounds. It is functionally related to mangosteen.
Mangosteen-7-O-glucoside has been reported in licorice, gromwell, and other organisms with relevant data. See also: closely related Astragalus root (partial). - Mangosteen-7-O-β-D-glucoside is a natural flavonoid glycoside isolated from Astragalus root, a traditional Chinese medicine with neuroprotective effects [1][2]. - Its protective effect against cerebral ischemia-reperfusion injury is mediated through two different pathways: in vivo, it regulates the NO/Cav-1/MMPs pathway to protect the integrity of the blood-brain barrier and reduce oxidative stress; in vitro experiments show that it can activate the SIRT1/FOXO1/PGC-1α pathway, thereby alleviating OGD/R-induced neuronal oxidative stress and apoptosis [1][2] - The dose-dependent efficacy of Calycosin-7-O-β-D-glucoside in in vitro and in vivo models suggests that it may be a promising candidate drug for the treatment of ischemic stroke [1][2] |
| Molecular Formula |
C22H22O10
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|---|---|
| Molecular Weight |
446.4041
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| Exact Mass |
446.121
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| CAS # |
20633-67-4
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| PubChem CID |
5318267
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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 |
745.2±60.0 °C at 760 mmHg
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| Flash Point |
262.0±26.4 °C
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| Vapour Pressure |
0.0±2.6 mmHg at 25°C
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| Index of Refraction |
1.675
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| LogP |
0.09
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| Hydrogen Bond Donor Count |
5
|
| Hydrogen Bond Acceptor Count |
10
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| Rotatable Bond Count |
5
|
| Heavy Atom Count |
32
|
| Complexity |
698
|
| Defined Atom Stereocenter Count |
5
|
| SMILES |
COC1=C(C=C(C=C1)C2=COC3=C(C2=O)C=CC(=C3)O[C@H]4[C@@H]([C@H]([C@@H]([C@H](O4)CO)O)O)O)O
|
| InChi Key |
WACBUPFEGWUGPB-MIUGBVLSSA-N
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| InChi Code |
InChI=1S/C22H22O10/c1-29-15-5-2-10(6-14(15)24)13-9-30-16-7-11(3-4-12(16)18(13)25)31-22-21(28)20(27)19(26)17(8-23)32-22/h2-7,9,17,19-24,26-28H,8H2,1H3/t17-,19-,20+,21-,22-/m1/s1
|
| Chemical Name |
3-(3-hydroxy-4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one
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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 |
| 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) |
DMSO : ≥ 100 mg/mL (~224.01 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (5.60 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 (5.60 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 (5.60 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.2401 mL | 11.2007 mL | 22.4014 mL | |
| 5 mM | 0.4480 mL | 2.2401 mL | 4.4803 mL | |
| 10 mM | 0.2240 mL | 1.1201 mL | 2.2401 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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