| Size | Price | Stock | Qty |
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| 500mg |
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| 1g |
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| 2g |
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| Other Sizes |
| Targets |
Cyclooxygenase-2 (COX-2) (IC₅₀: 3.5 µg/mL (19.23 µM)). [2]
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| ln Vitro |
Syringaldehyde has an IC50 of 3.5 μg/mL and inhibits COX-2 activity in a dose-dependent manner[2]
Syringaldehyde moderately inhibited COX-2 enzyme activity in a cell-based assay using lipopolysaccharide (LPS)-stimulated mouse macrophage RAW 264.7 cells, with an IC₅₀ value of 3.5 µg/mL (19.23 µM). The inhibition was dose-dependent. In a cellular antioxidant assay using human promyelocytic HL-60 cells stimulated with phorbol 12-myristate 13-acetate (PMA), syringaldehyde showed no antioxidant activity (inactive in the DCFH-DA assay). Cytotoxicity assays in both RAW 264.7 and HL-60 cells indicated that syringaldehyde was not cytotoxic at concentrations up to 25 µg/mL (RAW 264.7) and 31.25 µg/mL (HL-60), respectively. [2] |
| ln Vivo |
In a rat model of diabetes caused by streptozotocin, syringaldehyde exhibits antihyperglycemic properties. Syringaldehyde has been shown to have anti-inflammatory properties in addition to its antioxidant capacity. This is because it has been shown to inhibit cyclooxygenase-2 (COX-2) in mouse macrophage cell lines [1].
Pre- and co-treatment with Syringaldehyde (SYD) at 25 and 50 mg/kg significantly attenuated the increase in heart weight and heart weight/tibia length ratio induced by isoproterenol (ISO) in rats. SYD treatment (12.5, 25, 50 mg/kg) dose-dependently reduced the elevated serum levels of cardiac marker enzymes (CK-MB, LDH, AST, ALT) and cardiac troponin I (cTnI) in ISO-induced myocardial infarcted rats. SYD treatment significantly decreased the elevated levels of malondialdehyde (MDA) and protein carbonyl (PC), markers of lipid and protein oxidation, in the heart tissue of ISO-treated rats. SYD administration restored the depleted levels of reduced glutathione (GSH) and the activities of antioxidant enzymes (SOD, catalase, GPx, GST, GR) in the cardiac tissue of ISO-challenged rats. The total antioxidant capacity (TAC) of plasma, assessed by ABTS⁺ radical scavenging, was significantly improved by SYD treatment in ISO-induced rats. SYD treatment attenuated the ISO-induced alterations in the activities of membrane-bound ATPases (increased Na⁺/K⁺ ATPase and decreased Ca²⁺ ATPase activity) in cardiac tissue. SYD pre- and co-treatment significantly reduced the elevated serum levels of pro-inflammatory cytokines (TNF-α and IL-6) and cardiac nitric oxide (NO) levels in ISO-induced rats. Scanning electron microscopy revealed that SYD treatment ameliorated the ISO-induced morphological damage (bleb formation) in rat erythrocytes (RBCs). Triphenyltetrazolium chloride (TTC) staining showed that SYD treatment dose-dependently reduced the myocardial infarct size in ISO-induced rats. Histopathological examination demonstrated that SYD treatment attenuated ISO-induced myocardial damage, including necrosis, inflammatory cell infiltration, loss of transverse striations, myofibrillar degeneration, and edema, in a dose-dependent manner. [1] |
| Enzyme Assay |
The activity of lactate dehydrogenase (LDH) in serum was assayed according to the method of Kornberg.
The activities of alanine transaminase (ALT) and aspartate transaminase (AST) in serum were evaluated using the Reitman & Frankel method. Superoxide dismutase (SOD) activity in heart tissue homogenate was measured by the method of Marklund and Marklund. Catalase activity was determined following the protocol of Claiborne. Glutathione peroxidase (GPx) activity was assessed according to the Flohe and Gunzler method. Glutathione-S-transferase (GST) activity was evaluated by the method described by Habig. Glutathione reductase (GR) activity was evaluated by the method of Carlberg and Mannervik. The activities of Na⁺/K⁺ ATPase and Ca²⁺ ATPase in tissue homogenate were assayed using methods devised by Bonting, and Hjertén and Pan, respectively. [1] |
| Cell Assay |
COX-2 Inhibition Assay: Mouse macrophage RAW 264.7 cells were seeded in 96-well plates and cultured. Cells were stimulated with LPS to induce COX-2 expression. After removing LPS, cells were treated with different concentrations of syringaldehyde for 2 hours. Arachidonic acid was then added, and the cells were incubated further. The amount of prostaglandin E₂ (PGE₂) released into the medium was quantified using an enzyme immunoassay kit to determine COX-2 activity.
Antioxidant Activity Assay (DCFH-DA): Human promyelocytic HL-60 cells were seeded in 96-well plates. Cells were pretreated with different concentrations of syringaldehyde for 30 minutes, then stimulated with PMA for 30 minutes. The fluorescent probe DCFH-DA was added, and after incubation, the fluorescence intensity of the oxidized product (DCF) was measured using a plate reader with excitation at 485 nm and emission at 530 nm. The ability to inhibit reactive oxygen species (ROS)-catalyzed oxidation of DCFH was calculated. Cytotoxicity Assay (Neutral Red): RAW 264.7 cells were seeded in 96-well plates, treated with different concentrations of syringaldehyde for 48 hours. Neutral red dye solution was added, and after incubation and washing, the incorporated dye was liberated from viable cells using acidified isopropanol. Absorbance was measured at 490 nm to determine cell viability. Cytotoxicity Assay (XTT): HL-60 cells were seeded, treated with syringaldehyde for 48 hours. XTT-PMS solution was added, and after incubation, the absorbance at 450 nm was measured to determine cell viability. [2] |
| Animal Protocol |
Adult male Wistar rats (180-220 g) were randomly divided into six groups (n=6).
Group 1 (Control): Received vehicle orally for 21 days. Group 2 (SYD alone): Received Syringaldehyde (SYD) orally at 50 mg/kg body weight for 21 days. Group 3 (ISO alone): Received vehicle for 21 days, followed by two subcutaneous injections of isoproterenol (ISO, 100 mg/kg) on the 20th and 21st day at a 24-hour interval. Groups 4, 5, 6 (SYD + ISO): Received SYD orally at 12.5, 25, or 50 mg/kg body weight, respectively, for 21 days, along with ISO injections on the 20th and 21st day. SYD was dissolved in saline for oral administration. On the 22nd day (24 hours after the second ISO injection), rats were sacrificed. Blood and heart tissues were collected for biochemical, histological, and morphological analyses. [1] |
| Toxicity/Toxicokinetics |
Neutrophil viability assays showed that eugenol at concentrations up to 25 µg/mL had no cytotoxic effect on mouse RAW 264.7 macrophages. XTT cell viability assays showed that eugenol at concentrations up to 31.25 µg/mL had no cytotoxic effect on human promyelocytes HL-60. [2]
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| References |
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| Additional Infomation |
Syringaldehyde is a hydroxybenzaldehyde, a compound of 4-hydroxybenzaldehyde with methoxy groups substituted at the 3 and 5 positions. It was isolated from Pisonia aculeata and Panax japonicus var. major and possesses hypoglycemic activity. It is both a hypoglycemic agent and a plant metabolite. It is a hydroxybenzaldehyde and a dimethoxybenzene. Syringaldehyde has been reported to exist in Rhinacanthus nasutus, Magnolia officinalis, and other organisms with relevant data. Syringaldehyde is a metabolite found in or produced by Saccharomyces cerevisiae. Syringaldehyde (SYD) is a polyphenolic compound belonging to the flavonoid class. This study investigated the protective effect of syringaldehyde against isoproterenol (ISO)-induced myocardial infarction in rats, a model that mimics the pathophysiological process of human myocardial infarction.
The mechanism by which eugenol exerts its cardioprotective effect may include its antioxidant properties (scavenging reactive oxygen species, reducing lipid/protein oxidation, and enhancing endogenous antioxidant defense), anti-inflammatory effects (reducing TNF-α, IL-6, and NO), and membrane stabilizing activity (regulating ATPase function). Studies have found that eugenol has a protective effect. The results showed that the efficacy of eugenol was dose-dependent, with doses of 25 and 50 mg/kg being more effective. This study concluded that foods rich in eugenol may help reduce oxidative damage in cardiovascular disease, but further research is needed to evaluate its clinical application value in humans. [1] Eugenol was isolated from the ethanol extract of the truffle fungus Elaphomyces granulatus by bioactivity-guided fractionation. This study is the first to report the presence of eugenol in Elaphomyces granulatus and its inhibitory activity against COX-2. Studies have shown that eugenol contributes to the anti-inflammatory effect of the fungal extract, but it lacks antioxidant activity in the cell assays used. [2] |
| Molecular Formula |
C₉H₁₀O₄
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|---|---|
| Molecular Weight |
182.17
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| Exact Mass |
182.057
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| CAS # |
134-96-3
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| PubChem CID |
8655
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| Appearance |
Light brown to brown solid powder
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| Density |
1.2±0.1 g/cm3
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| Boiling Point |
322.1±37.0 °C at 760 mmHg
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| Melting Point |
110-113 °C(lit.)
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| Flash Point |
130.1±20.0 °C
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| Vapour Pressure |
0.0±0.7 mmHg at 25°C
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| Index of Refraction |
1.568
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| LogP |
0.86
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
3
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| Heavy Atom Count |
13
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| Complexity |
157
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
KCDXJAYRVLXPFO-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C9H10O4/c1-12-7-3-6(5-10)4-8(13-2)9(7)11/h3-5,11H,1-2H3
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| Chemical Name |
4-hydroxy-3,5-dimethoxybenzaldehyde
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| Synonyms |
VND3207 Syringaldehyde NSC-41153NSC41153NSC 41153 NSC-41153 SM707SM 707 SM-707VND-3207VND 3207
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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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture. |
| 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 (~548.94 mM)
H2O : < 0.1 mg/mL |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (13.72 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 (13.72 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 (13.72 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 | 5.4894 mL | 27.4469 mL | 54.8938 mL | |
| 5 mM | 1.0979 mL | 5.4894 mL | 10.9788 mL | |
| 10 mM | 0.5489 mL | 2.7447 mL | 5.4894 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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