(+)-Medioresinol
Based on 1 publication(s) in Google Scholar
(+)-Medioresinol is a furofuran-type lignan with antifungal and antibacterial properties. (+)-Medioresinol synergizes with antibiotics to exert antimicrobial and antibiofilm effects. (+)-Medioresinol induces intracellular ROS accumulation and mitochondrial-mediated apoptosis in Candida albicans. (+)-Medioresinol inhibits LPS (HY-D1056)-stimulated IL-12p40 production. (+)-Medioresinol is a PGC-1α activator that protects against endothelial cell pyroptosis in ischemic stroke via the PPARα-GOT1 axis. (+)-Medioresinol can be used in research on fungal and bacterial infection, inflammation, and ischemic stroke.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 99.13%
- CAS 番号: 40957-99-1
- 分子式: C21H24O7
- 分子量:388.41
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保管条件:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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生物活性
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化学情報
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溶剤 & 溶解度
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MedChemExpress（MCE）の使用を引用している文献 (+)-Medioresinol
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生物活性
製品説明
IC50 & Target
[3]|
IL-12 |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
>30 μM
Compound: 8
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Cytotoxicity against human A549 cells by SRB assay
Cytotoxicity against human A549 cells by SRB assay
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[PMID: 26988298] |
| BMDC | IC50 |
2 μM
Compound: 13
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Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated IL-12p40 production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated IL-12p40 production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
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[PMID: 23484668] |
| BMDC | IC50 |
20.87 μM
Compound: 13
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Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated IL12 production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated IL12 production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
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[PMID: 23484668] |
| BMDC | IC50 |
22.29 μM
Compound: 13
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Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated TNF-alpha production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
Antiinflammatory activity in C57BL/6 mouse BMDCs assessed as inhibition of LPS-stimulated TNF-alpha production treated 1 hr before LPS challenge measured 18 hrs post stimulation by ELISA
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[PMID: 23484668] |
| BV-2 | IC50 |
45.59 μM
Compound: 8
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Anti-neuroinflammatory activity in LPS-activated mouse BV2 cells assessed as inhibition of NO production after 24 hrs by Griess assay
Anti-neuroinflammatory activity in LPS-activated mouse BV2 cells assessed as inhibition of NO production after 24 hrs by Griess assay
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[PMID: 26988298] |
| RAW264.7 | IC50 |
0.245 mM
Compound: 7
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Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs
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[PMID: 18986199] |
| RAW264.7 | IC50 |
0.245 μM/mL
Compound: 7
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Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs
Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs
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[PMID: 18986199] |
| SK-MEL-2 | IC50 |
>30 μM
Compound: 8
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Cytotoxicity against human SK-MEL-2 cells by SRB assay
Cytotoxicity against human SK-MEL-2 cells by SRB assay
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[PMID: 26988298] |
| SK-OV-3 | IC50 |
>30 μM
Compound: 8
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Cytotoxicity against human SKOV3 cells by SRB assay
Cytotoxicity against human SKOV3 cells by SRB assay
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[PMID: 26988298] |
| XF498 | IC50 |
>30 μM
Compound: 8
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Cytotoxicity against human XF498 cells by SRB assay
Cytotoxicity against human XF498 cells by SRB assay
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[PMID: 26988298] |
体外実験
(+)-Medioresinol (18 h) exerts antibacterial activity anginst E. faecium ATCC 19434, S. aureus ATCC 25923, P. acnes ATCC 6919, E. coli O-157 ATCC 43895, E. coli ATCC 25922, P. aeruginosa ATCC 27853, with MICs of 2.5, 5, 5, 5, 2.5, 20 µg/mL[1].
(+)-Medioresinol has enhanced antibacterial effect against E. coli in combination with Cefotaxime (HY-A0088A) and Chloramphenicol (HY-B0239), synergistic effect against Staphylococcus aureus in combination with Ampicillin (HY-B0522) and Cefotaxime[1].
(+)-Medioresinol (MIC/FIC x 1, x 4, x 10) inhibits biofilm formation against E. faecium ATCC 19434, S. aureus ATCC 25923, P. acnes ATCC 6919, E. coli O-157 ATCC 43895, E. coli ATCC 25922, P. aeruginosa ATCC 27853 in combination with Ampicillin, Cefotaxime, Chloramphenicol[1].
(+)-Medioresinol exerts antifungal activity against C. albicans, C. parapsilosis, T. beigelii, M. furfur, with MICs of 3.125-6.25 µg/mL[2].
(+)-Medioresinol (3.125 μg/mL, 2-4 h) arrests cells in G0/G1 phase, increases the accumulation of intracellular ROS levels, induces depolarization of MMP in C. albicans cells[2].
(+)-Medioresinol (3.125 μg/mL, 2-4 h) induces mitochondrial release of Cyt c, metacaspase activation and DNA and nuclear damage, increases phosphatidylserine externalization and side scatter (SSC), decreases forward scatter (FSC) in C. albicans cells[2].
(+)-Medioresinol (Compound 13) shows significant inhibitory activity on IL-12p40, with an IC50 of 2 μM in LPS-stimulated BMDCs[3].
(+)-Medioresinol (60-120 μM, 24 h) counteracts the decreased vitality and increased NT-proBNP levels caused by oxygen and glucose deprivation (OGD) in H9c2 cells[4].
(+)-Medioresinol (60-120 μM, 24 h) reduces ROS, TNF-α, and IL-1β levels, increases PI3K, p-AKT, and p-mTOR levels in OGD H9c2 cells[4].
(+)-Medioresinol (5-20 μM, 3-15 h) reduces the secretion of LDH, promotes the expression of PGC-1α and the protein expression of ZO-1 and Occludin, activates PGC-1α protected ischemia-induced brain injury in bEnd.3 cells[5].
(+)-Medioresinol (20 μM, 15 h) inhibits pyroptosis of endothelial cells to protect the integrity of BBB by regulating phenylalanine metabolism and PGC-1α-mediated PAH and GOT1 expression in bEnd.3 cells caused by oxygen-glucose deprivation (OGD)[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:C. albicans cells
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Concentration:3.125 μg/mL
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Incubation Time:4 h
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Result:Arrested cells in G0/G1 phase.
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Cell Line:C. albicans cells
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Concentration:3.125 μg/mL
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Incubation Time:2 h
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Result:Induced ROS accumulation related to apoptosis.
Reduced the fluorescence of FL-2 and slightly increased the fluorescence of FL-1, induced depolarization of mitochondrial membrane potential.
Reduced the relative level of Cyt c in mitochondria and increased the relative level of Cyt c in the cytoplasm.
Induced metacaspase activation, increased phosphatidylserine externalization, decreased FSC, increased SSC.
Induced DNA and nuclear damage.
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Cell Line:OGD H9c2 cells
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Concentration:120 μM
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Incubation Time:24 h
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Result:Increased PI3K, p-AKT, and p-mTOR levels.
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Cell Line:bEnd.3 cells
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Concentration:5, 10, 20 μM
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Incubation Time:3, 15 h
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Result:Promoted the protein expression of ZO-1 and Occludin.
Reduced the expressions of pyroptosis-associated proteins (NLRP3, ASC, cleaved caspase-1, IL-1β and GSDMD-NT).
Increased the expression of PAH and GOT1.
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Cell Line:bEnd.3 cells
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Concentration:20 μM
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Incubation Time:15 h
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Result:Reduced OGD induced mtROS expression, reversed OGD-induced mitochondrial membrane potential reduction, reduced infarct volume and NLRP3+CD31+ cells number in the peri-infarct cortex at 48 h after surgery.
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Cell Line:bEnd.3 cells
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Concentration:20 μM
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Incubation Time:4 h
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Result:Increased PGC-1α mRNA expression, while has no effect on the mRNA expression of PGC-1β and PPRC.
体内実験
(+)-Medioresinol (1-10 mg/kg, i.v., at 2 h and 24 h after ischemia) promotes long-term functional recovery of mice with ischemia. in tMCAO mice model[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male ICR mice (25-30 g, 8-10 weeks old) model[1]
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Dosage:1 mg/kg or 10 mg/kg
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Administration:i.v., at 2 h and 24 h after ischemia
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Result:Reduced infarct volume tested by TTC staining, decreased brain swelling volume and brain water content, decreased the area of IgG extravasation, reversed the reduction of ZO-1 and Occludin, attenuated ischemia-caused decrease in the protein expression of Occludin in cerebral microvascular endothelial cells.
Decreased protein expression level of pyroptosis-associated markers, NLRP3+ CD31+ cells in peri-infarct cortex, the ASC expression in cerebral microvascular endothelial cells.
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Animal Model:Focal cerebral ischemia procedure (tMCAO) male ICR mice (25-30 g, 8-10 weeks old) model[1]
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Dosage:1 mg/kg or 10 mg/kg
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Administration:i.v., at 2 h and 24 h after ischemia
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Result:Decreased infarct sizes and mortality, increased the time in Rotarod test, and decreased the number of right turns and the scores of mNSS.
化学情報
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CAS 番号 40957-99-1
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性状 Solid
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分子量 388.41
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分子式 C21H24O7
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Color White to off-white
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SMILES
COC1=C(O)C(OC)=CC([C@]2([H])[C@]3([H])[C@@](CO2)([H])[C@](C4=CC(OC)=C(C=C4)O)([H])OC3)=C1
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Structure Classification
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Initial Source
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Publications (1)
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Journal Impact Factor
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Most Recent
溶剤 & 溶解度
体外:
DMSO : 50 mg/mL (128.73 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
体内:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 1.25 mg/mL (3.22 mM); Clear solution
This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (12.5 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: ≥ 1.25 mg/mL (3.22 mM); Clear solution
This protocol yields a clear solution of ≥ 1.25 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (12.5 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL. * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
プロトコル
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
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Detection of Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
純度とドキュメンテーション
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データシート (292 KB)
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取扱説明書 (2659 KB)
参考文献
[1]. Ji Hong Hwang, et al. (+)-Medioresinol leads to intracellular ROS accumulation and mitochondria-mediated apoptotic cell death in Candida albicans. Biochimie. 2012 Aug;94(8):1784-93. [Content Brief]
[2]. Ji Hong Hwang, et al. Synergistic antibacterial and antibiofilm effect between (+)-medioresinol and antibiotics in vitro. Appl Biochem Biotechnol. 2013 Aug;170(8):1934-41. [Content Brief]
[3]. Nhiem NX, et al. Diarylheptanoids and flavonoids from viscum album inhibit LPS-stimulated production of pro-inflammatory cytokines in bone marrow-derived dendritic cells. J Nat Prod. 2013 Apr 26;76(4):495-502. [Content Brief]
[4]. Qin X, et al. Medioresinol from Eucommiae cortex improves myocardial infarction-induced heart failure through activation of the PI3K/AKT/mTOR pathway: A network analysis and experimental study. PLoS One. 2024 Sep 27;19(9):e0311143. [Content Brief]
[5]. Wang Y, et al. Medioresinol as a novel PGC-1α activator prevents pyroptosis of endothelial cells in ischemic stroke through PPARα-GOT1 axis. Pharmacol Res. 2021 Jul;169:105640. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.5746 mL | 12.8730 mL | 25.7460 mL | 64.3650 mL |
| 5 mM | 0.5149 mL | 2.5746 mL | 5.1492 mL | 12.8730 mL | |
| 10 mM | 0.2575 mL | 1.2873 mL | 2.5746 mL | 6.4365 mL | |
| 15 mM | 0.1716 mL | 0.8582 mL | 1.7164 mL | 4.2910 mL | |
| 20 mM | 0.1287 mL | 0.6436 mL | 1.2873 mL | 3.2182 mL | |
| 25 mM | 0.1030 mL | 0.5149 mL | 1.0298 mL | 2.5746 mL | |
| 30 mM | 0.0858 mL | 0.4291 mL | 0.8582 mL | 2.1455 mL | |
| 40 mM | 0.0644 mL | 0.3218 mL | 0.6436 mL | 1.6091 mL | |
| 50 mM | 0.0515 mL | 0.2575 mL | 0.5149 mL | 1.2873 mL | |
| 60 mM | 0.0429 mL | 0.2145 mL | 0.4291 mL | 1.0727 mL | |
| 80 mM | 0.0322 mL | 0.1609 mL | 0.3218 mL | 0.8046 mL | |
| 100 mM | 0.0257 mL | 0.1287 mL | 0.2575 mL | 0.6436 mL |
(+)-Medioresinol 関連分類
HY-N3307 関連分類
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