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    Syringic acid
    Information
    CAS No. 530-57-4 Price $30 / 20mg
    Catalog No.CFN98884Purity>=98%
    Molecular Weight198.2 Type of CompoundPhenols
    FormulaC9H10O5Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Syringic acid is a potential antioxidant used in traditional Chinese medicine and is an emerging nutraceutical. It has potential anti-angiogenic, anti-glycating, anti-hyperglycaemic,antimicrobial, fungitoxicity, neuroprotective, antimitogenic, chemo-sensitizing, anti-obesity, anti-inflammatory, anti-steatotic, and memory-enhancing properties. Syringic acid can ameliorate L-arginine methyl ester-induced hypertension by reducing oxidative stress, and can reduce the pancreatic damage induced by alloxan and stimulated β-cell regeneration in diabetic rats. Syringic acid can suppress hepatic fibrosis in chronic liver injury, it inhibits the activation of cultured hepatic stellate cells.
    Targets: Caspase | IFN-γ | IL Receptor | TNF-α | NF-kB | NO | Antifection
    In vitro:
    Pharm Biol. 2013 Sep;51(9):1110-24.
    Syringic acid from Tamarix aucheriana possesses antimitogenic and chemo-sensitizing activities in human colorectal cancer cells.[Pubmed: 23745612]
    For its variety of biological activities, Tamarix aucheriana (Decne.) Baum. (Tamaricaceae) has an extensive history as a traditional Arab medicine. Antimitogenic and chemo-sensitizing activities of Syringic acid (SA) were studied against human colorectal cancer.
    METHODS AND RESULTS:
    Chromatographic and spectral data were used for the isolation and identification of SA. MTT, flow cytometry, in vitro invasion and angiogenesis assays, fluoremetry, ELISA and Real Time qPCR were used to test antimitogenic and chemo-sensitizing activities of SA, cell cycle, apoptosis, proteasome and NFκB-DNA-binding activities, cancer cell invasion and angiogenesis, and expression of cell cycle/apoptosis-related genes.SA showed a time- and dose-dependent (IC₅₀ = 0.95-1.2 mg mL⁻1) antimitogenic effect against cancer cells with little cytotoxicity on normal fibroblasts (≤20%). SA-altered cell cycle (S/G2-M or G1/G2-M phases) in a time-dependent manner, induced apoptosis, inhibited DNA-binding activity of NFκB (p ≤ 0.0001), chymotrypsin-like/PGPH (peptidyl-glutamyl peptide-hydrolyzing) (p ≤ 0.0001) and the trypsin-like (p ≤ 0.002) activities of 26S proteasome and angiogenesis. SA also differentially sensitized cancer cells to standard chemotherapies with a marked increase in their sensitivity to camptothecin (500-fold), 5FU (20,000-fold), doxorubicin (210-fold), taxol (3134-fold), vinblastine (1000-fold), vincristine (130-fold) and amsacrine (107-fold) compared to standard drugs alone. SA exerted its chemotherapeutic and chemo-sensitizing effects through an array of mechanisms including cell-cycle arrest, apoptosis induction, inhibition of cell proliferation, cell migration, angiogenesis, NFκB DNA-binding and proteasome activities.
    CONCLUSIONS:
    These results demonstrate the potential of SA as an antimitogenic and chemo-sensitizing agent for human colorectal cancer.
    J. Agr. Sci., 2009, 1(2):15-20.
    In Vitro Antimicrobial Activity and Fungitoxicity of Syringic Acid, Caffeic Acid and 4-hydroxybenzoic Acid against Ganoderma Boninense.[Reference: WebLink]
    This paper discusses the in vitro antimicrobial activity and fungitoxicity of Syringic acid, caffeic acid and4-hydroxybenzoic acid which is found in oil palm root.
    METHODS AND RESULTS:
    Experiments were observed for fourteen days, repeated at leastthree times and data were recorded daily. The antimicrobial activities and fungitoxicity of the phenolics againstGanoderma boninense were expressed in inhibition of radial growth of G. boninense on PDA ameliorated with the threedifferent phenolics with a range concentration of 0.5-2.5 mg/ml. Syringic acid was found to be very fungitoxic to G.boninense even at concentration of 0.5 mg/ml, the lowest concentration tested in this experiment. When theconcentration is increase to 1.0mg/ml of Syringic acid, the pathogen is inhibited.
    CONCLUSIONS:
    Caffeic acid and 4-hydroxybenzoicacid were having inhibitory effect with the highest concentration tested; 2.5mg/ml strongly inhibited the growth of G.boninense in comparison to the control.
    In vivo:
    Turk J Med Sci. 2015;45(1):233-40.
    The protective effect of syringic acid on ischemia injury in rat brain.[Pubmed: 25790559]
    Brain ischemia and treatment are important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most significant causes of damage. Currently there are studies on many chemopreventive agents to prevent cerebral ischemia damage. Our aim is to research the preventive effect of the active ingredient in Syringic acid, previously unstudied, on oxidative damage in cerebral ischemia.
    METHODS AND RESULTS:
    The rats were randomly divided into 4 groups: control group (no medication or surgical procedure), sham group (artery occlusion), artery occlusion + Syringic acid group sacrificed at 6 h, and artery occlusion + Syringic acid group sacrificed at 24 h. Obtained brain tissue from the right hemisphere was investigated histopathologically and for tissue biochemistry. Superoxide dismutase and nuclear respiratory factor 1 values decreased after ischemia and they increased after Syringic acid treatment, while increased malondialdehyde levels after ischemia were reduced after treatment. Caspase-3 and caspase-9 values increased after ischemia and decreased after treatment; this reduction was more pronounced at 24 h.
    CONCLUSIONS:
    Our study revealed that Syringic acid treatment in cerebral ischemia reduced oxidative stress and neuronal degeneration. In the light of the biochemical and histopathologic results of the present study, we think that Syringic acid treatment may be an alternative treatment method.
    Inflammation. 2015 Apr 23.
    The Neuroprotective Effect of Syringic Acid on Spinal Cord Ischemia/Reperfusion Injury in Rats.[Pubmed: 25903968]
    Acute arterial occlusions via different vascular pathologies are the main causes of spinal cord ischemia. We investigated neuroprotective effects of Syringic acid on spinal cord ischemia injury in rats.
    METHODS AND RESULTS:
    Rats were divided into four groups: (I) sham-operated control rats, (II) spinal cord ischemia group, (III) spinal cord ischemia group performed Syringic acid, and (IV) spinal cord ischemia group performed methylprednisolone intraperitoneally. Spinal cord ischemia was performed by the infrarenal aorta cross-clamping model. The spinal cord was removed after the procedure. The biochemical and histopathological changes were observed within the samples. Functional assessment was performed for neurological deficit scores. A significant decrease was seen in malondialdehyde levels in group III as compared to group II (P < 0.05). Besides these, nuclear respiratory factor-1 and superoxide dismutase activity of group III were significantly higher than group II (P < 0.05). In histopathological samples, when group III was compared with group II, there was a significant decrease in numbers of apoptotic neurons (P < 0.05). In immunohistochemical staining, BECN1 and caspase-3-immunopositive neurons were significantly decreased in group III compared with group II (P < 0.05). The neurological deficit scores of group III were significantly higher than group II at twenty-fourth hour of ischemia (P < 0.05).
    CONCLUSIONS:
    Our study revealed that Syringic acid pretreatment in spinal cord ischemia/reperfusion reduced oxidative stress and neuronal degeneration as a neuroprotective agent. Ultrastructural studies are required for Syringic acid to be developed as a promising therapeutic agent to be utilized for human spinal cord ischemia in the future.
    Biomedicine & Preventive Nutrition, 2014, 4(4):595-602.
    Antihyperglycemic effect of syringic acid on attenuating the key enzymes of carbohydrate metabolism in experimental diabetic rats.[Reference: WebLink]
    Diabetes mellitus is one of the most common endocrine entities, which coexist with defect in carbohydrate metabolism. The Indian traditional system of medicine prescribed plant phytochemical therapies for diseases including diabetes mellitus.
    METHODS AND RESULTS:
    The present study was aimed to evaluate the therapeutic potential of Syringic acid (SA) by assaying the activities of key enzymes of carbohydrate metabolism in experimental diabetic rats. Diabetes was induced into male albino Wistar rats by intraperitoneal administration of alloxan (150mg/kg). SA was administered to diabetic rats intragastrically at 25, 50 and 100mg/kg b.w daily once for 30days. The levels of plasma glucose, insulin, hemoglobin (Hb), glycated hemoglobin (HbA1c) and glycogen, levels of carbohydrate metabolic enzymes, liver and kidney markers were evaluated. Oral administration of SA (50mg/kg) for 30days, dose dependently improved the glycemic status in diabetic rats. The levels of insulin, Hb and glycogen increased with significant decrease in glucose and HbA1clevels in SA treated rats. The altered activities of carbohydrate metabolic enzymes, hepatic and renal marker were restored to near normal. Histopathological analysis of pancreas revealed that treatment with SA reduced the pancreatic damage induced by alloxan and stimulated β-cell regeneration in diabetic rats.
    CONCLUSIONS:
    The present findings suggest the antihyperglycemic effect of SA and its therapeutic potential for the management of diabetes.
    Syringic acid Description
    Source: The herbs of Michelia spaerantha C.Y.Wu
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.0454 mL 25.227 mL 50.4541 mL 100.9082 mL 126.1352 mL
    5 mM 1.0091 mL 5.0454 mL 10.0908 mL 20.1816 mL 25.227 mL
    10 mM 0.5045 mL 2.5227 mL 5.0454 mL 10.0908 mL 12.6135 mL
    50 mM 0.1009 mL 0.5045 mL 1.0091 mL 2.0182 mL 2.5227 mL
    100 mM 0.0505 mL 0.2523 mL 0.5045 mL 1.0091 mL 1.2614 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Animal Research:
    Food Funct. 2016 Feb;7(2):689-97.
    Anti-steatotic and anti-inflammatory roles of syringic acid in high-fat diet-induced obese mice.[Pubmed: 26838182 ]
    This study examined the effects of Syringic acid (SA) on obese diet-induced hepatic dysfunction.
    METHODS AND RESULTS:
    Mice were fed high-fat diet (HFD) with or without SA (0.05%, wt/wt) for 16 weeks. SA reduced the body weight, visceral fat mass, serum levels of leptin, TNFα, IFNγ, IL-6 and MCP-1, insulin resistance, hepatic lipid content, droplets and early fibrosis, whereas it elevated the circulation of adiponectin. SA down-regulated lipogenic genes (Cidea, Pparγ, Srebp-1c, Srebp-2, Hmgcr, Fasn) and inflammatory genes (Tlr4, Myd88, NF-κB, Tnfα, Il6), whereas it up-regulated fatty acid oxidation genes (Pparα, Acsl, Cpt1, Cpt2) in the liver. SA also decreased hepatic lipogenic enzyme activities and elevated fatty acid oxidation enzyme activities relative to the HFD group.
    CONCLUSIONS:
    These findings suggested that dietary SA possesses anti-obesity, anti-inflammatory and anti-steatotic effects via the regulation of lipid metabolic and inflammatory genes. SA is likely to be a new natural therapeutic agent for obesity or non-alcoholic liver disease.
    Int Surg. 2015 May;100(5):891-6.
    Antioxidant Activity of Syringic Acid Prevents Oxidative Stress in l-arginine-Induced Acute Pancreatitis: An Experimental Study on Rats.[Pubmed: 26011211]
    The aim of this study was to investigate the possible protective role of antioxidant treatment with Syringic acid (SA) on l-arginine-induced acute pancreatitis (AP) using biochemical and histopathologic approaches.
    METHODS AND RESULTS:
    A total of 30 rats were divided into 3 groups. The control group received normal saline intraperitoneally. The AP group was induced by 3.2 g/kg body weight l-arginine intraperitoneally, administered twice with an interval of 1 hour between administrations. The AP plus SA group, after having AP induced by 3.2 g/kg body weight l-arginine, was given SA (50 mg kg(-1)) in 2 parts within 24 hours. The rats were killed, and pancreatic tissue was removed and used in biochemical and histopathologic examinations. Compared with the control group, the mean pancreatic tissue total oxidant status level, oxidative stress index, and lipid hydroperoxide levels were significantly increased in the AP group, being 30.97 ± 7.13 (P < 0.05), 1.76 ± 0.34 (P < 0.0001), and 19.18 ± 4.91 (P < 0.01), respectively. However, mean total antioxidant status and sulfhydryl group levels were significantly decreased in the AP group compared with the control group, being 1.765 ± 0.21 (P < 0.0001) and 0.21 ± 0.04 (P < 0.0001), respectively. SA reduces oxidative stress markers and has antioxidant effects.
    CONCLUSIONS:
    It also augments antioxidant capacity in l-arginine-induced acute toxicity of pancreas in rats.
    Naunyn Schmiedebergs Arch Pharmacol. 2012 Dec;385(12):1175-84.
    Syringic acid ameliorates (L)-NAME-induced hypertension by reducing oxidative stress.[Pubmed: 23079793]
    The objective of the present study was to investigate the effects of Syringic acid (SA), a phenolic acid, on N(ω)-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats.
    METHODS AND RESULTS:
    Hypertension was induced in adult male albino rats by oral administration of L-NAME (40 mg/kg/day) dissolved in drinking water daily for 4 weeks. Rats were treated with different doses of SA (25, 50, and 100 mg/kg body weight (b.w.)). Systolic blood pressure of control and experimental rats was recorded. Plasma nitric oxide metabolites (NOx), lipid peroxidative products such as thiobarbituric acid reactive substances, lipid hydroperoxides, conjugated dienes, and antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, vitamin C, vitamin E, and reduced glutathione were estimated in erythrocytes, plasma, and tissues of experimental rats. Hepatic marker enzymes such as aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase and renal functional markers such as urea, uric acid, and creatinine were also estimated in serum. The increased levels of blood pressure, lipid peroxidation products, hepatic and renal function markers, and the decreased level of NOx and antioxidants in L-NAME-induced hypertensive rats were reversed upon SA treatment. The protective effect at the dose of the three tested doses (25, 50, and 100 mg/kg) of SA at a dose of 50 mg/kg b.w. exerts optimum protection. Biochemical findings are substantiated by the histological observation.
    CONCLUSIONS:
    The protective effects of SA are mediated by reducing oxidative stress and retaining the bioavailability of NO in the cardiovascular system.
    Biol Pharm Bull. 2010;33(6):983-7.
    Hepatoprotective effect of syringic acid and vanillic acid on CCl4-induced liver injury.[Pubmed: 20522963]
    The mycelia of the edible mushroom Lentinula edodes can be cultured in solid medium containing lignin, and the hot-water extracts (L.E.M.) is commercially available as a nutritional supplement.
    METHODS AND RESULTS:
    During the cultivation, phenolic compounds, such as Syringic acid and vanillic acid, were produced by lignin-degrading peroxidase secreted from L. edodes mycelia. Since these compounds have radical scavenging activity, we examined their protective effect on oxidative stress in mice with CCl(4)-induced liver injury. We examined the hepatoprotective effect of Syringic acid and vanillic acid on CCl(4)-induced chronic liver injury in mice. The injection of CCl(4) into the peritoneal cavity caused an increase in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. The intravenous administration of Syringic acid and vanillic acid significantly decreased the levels of the transaminases. Four weeks of CCl(4) treatment caused a sufficiently excessive deposition of collagen fibrils. An examination of Azan-stained liver sections revealed that Syringic acid and vanillic acid obviously suppressed collagen accumulation and significantly decreased the hepatic hydroxyproline content, which is the quantitative marker of fibrosis. Both of these compounds inhibited the activation of cultured hepatic stellate cells, which play a central role in liver fibrogenesis, and maintained hepatocyte viability.
    CONCLUSIONS:
    These data suggest that the administration of Syringic acid and vanillic acid could suppress hepatic fibrosis in chronic liver injury.