Sophoricoside
(Synonyms: 槐角苷) 目录号 : GC31781
An isoflavone glycoside with diverse biological activities
Cas No.:152-95-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Kinase experiment: | Cells are incubated with the Sophoricoside for 1 h, and then incubated with PMACI for 2 h. The reaction is stopped by cooling the tubes in ice. The cells are separated from the released histamine by centrifugation at 400×g for 5 min at 4°C. The histamine levels are measured by ELISA using a histamine assay kit according to the manufacturer’s directions. Duplicate aliquots of supernatant are measured for each sample[1]. |
Cell experiment: | To test the cell viability by each concentration of Sophoricoside, the MTT colorimetric assay is performed. Briefly, HMC-1 cells (3×105 cells/well) are incubated with Sophoricoside (1 to 50 μM) for 12 h. After the addition of MTT solution, the cells are incubated at 37°C for 4 h. The crystallized MTT (formazan) is dissolved in dimethyl sulfoxide and the absorbance is measured at 540 nm[1]. |
Animal experiment: | BALB/c mice (5 weeks, 19 to 20 g) are used in this study. The dorsal skin of the BALB/c mice (n=6) is shaved and treated with a depilatory prior to the experiment. The mice are sensitized with 100 μL of 0.15% DNCB in acetone-olive oil (3:1) applied to the dorsal skin twice per week for 5 weeks. Control mice receive vehicle (acetone/olive oil=3:1). After 3 weeks, Sophoricoside (2 mg/kg) is orally administered 2 weeks until the end of the experiment[1]. |
References: [1]. Kim SJ, et al. The ameliorative effect of sophoricoside on mast cell-mediated allergic inflammation in vivo and in vitro. Molecules. 2013 May 22;18(5):6113-27. | |
Sophoricoside is a polyketide synthase-derived isoflavone glycoside that has been found in S. japonica and has diverse biological activities.1,2,3,4,5 It inhibits lipid accumulation induced by oleic acid in HepG2 cells and stimulates glucose uptake in C2C12 mouse skeletal muscle myoblasts when used at a concentration of 10 ?M.2 Sophoricoside (2 mg/kg) reduces scratching behavior induced by compound 48/80 or histamine in mice, as well as reduces serum levels of IgE in a mouse model of atopic dermatitis.3 It increases serum levels of osteocalcin and alkaline phosphatase (ALP) and restores mechanical bone hardness in an ovariectomized rat model of osteoporosis.4 Sophoricoside (80 and 160 mg/kg) decreases hepatic cholesterol and triglyceride levels, serum LDL and apolipoprotein B levels, and hepatic injury in a mouse model of fructose-induced liver injury.5
1.Trantas, E.A., Koffas, M.A.G., Xu, P., et al.When plants produce not enough or at all: Metabolic engineering of flavonoids in microbial hostsFront. Plant Sci.6(7)(2015) 2.Wu, C., Luan, H., Wang, S., et al.Modulation of lipogenesis and glucose consumption in HepG2 cells and C2C12 myotubes by sophoricosideMolecules18(12)15624-15635(2013) 3.Kim, S.-J., Lee, G.-Y., Jung, J.-W., et al.The ameliorative effect of sophoricoside on mast cell-mediated allergic inflammation in vivo and in vitroMolecules18(5)6113-6127(2013) 4.Abdallah, H.M., Al-Abd, A.M., Asaad, G.F., et al.Isolation of antiosteoporotic compounds from seeds of Sophora japonicaPLoS One9(6)e98559(2014) 5.Li, W., and Lu, Y.Hepatoprotective effects of sophoricoside against fructose-induced liver injury via regulating lipid metabolism, oxidation, and inflammation in miceJ. Food Sci.83(2)552-558(2018)
| Cas No. | 152-95-4 | SDF | |
| 别名 | 槐角苷 | ||
| Canonical SMILES | OC1=CC(O)=C(C(C(C2=CC=C(O[C@H]3[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O3)C=C2)=CO4)=O)C4=C1 | ||
| 分子式 | C21H20O10 | 分子量 | 432.38 |
| 溶解度 | DMSO : ≥ 150 mg/mL (346.92 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3128 mL | 11.5639 mL | 23.1278 mL |
| 5 mM | 0.4626 mL | 2.3128 mL | 4.6256 mL |
| 10 mM | 0.2313 mL | 1.1564 mL | 2.3128 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Sophoricoside attenuates lipopolysaccharide-induced acute lung injury by activating the AMPK/Nrf2 signaling axis
Sophoricoside (SOP), an isoflavone glycoside isolated from seed of Sophora japonica L., has been reported to have various pharmacological activities, including anti-cancer, anti-allergy and anti-inflammation. However, the effect of SOP on lipopolysaccharides (LPS)-acute lung injury (ALI) is completely unclear. Here, we found that SOP pretreatment significantly ameliorated LPS-induced pathological damage, tissue permeability, neutrophil infiltration and the production of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) in a murine model of ALI. Besides, SOP reduced the production of pro-inflammatory mediators such as iNOS, NO and inflammatory cytokines including TNF-α, IL-1β and IL-6 in LPS-stimulated RAW264.7 cells and bone marrow derived macrophages. Interestingly, treatment with SOP exhibited no effect on the activation of NF-κB and MAPKs in macrophages but prominently accelerated the expression and nuclear translocation of Nrf2. By using ML385, a specific Nrf2 inhibitor, we found that inhibition of Nrf2 abolished the inhibitory effect of SOP on LPS-induced iNOS expression, NO production as well as pro-inflammatory cytokine generation. SOP also activated AMPK, an upstream protein of Nrf2, under LPS stimuli. Furthermore, we demonstrated that the accelerated expression of Nrf2 induced by SOP was reversed by interference with the AMPK inhibitor Compound C. Taken together, our results suggested that SOP attenuated LPS-induced ALI in AMPK/Nrf2 dependent manner and indicated that SOP might be a potential therapeutic candidate for treating ALI/ARDS.
Sophoricoside from Styphnolobium japonicum improves experimental atopic dermatitis in mice
Background: Abnormal immune responses, specifically excessive differentiation of Th2 cells, are associated with the development of atopic dermatitis (AD). Sophoricoside, the genistein-4'-β-D-glucoside isolated from Styphnolobium japonicum, has previously demonstrated anti-inflammatory and immunosuppressive effects along with IL-3 and IL-5 inhibitory activities. Therefore, we speculated that sophoricoside could regulate AD by regulating abnormal immune responses.
Purpose: To investigate the role of sophoricoside on AD-like allergic skin inflammation induced by ovalbumin (OVA) or 2,4,6-trinitrochlorobenzene (TNCB) in mouse models.
Methods: Sophoricoside was isolated from the 70% ethanol extract of S. japonicum dried mature seeds. After being submitted to a purification process, its purity was assessed by high-performance liquid chromatography (HPLC). The effects of sophoricoside were determined in vivo by OVA- and TNCB-induced AD-like allergic skin inflammation in mice. Skin tissues were subjected with hematoxylin-eosin (H&E), Giemsa and toluidine blue staining. In vitro CD4+ T cell differentiation was performed and the levels of serum immunoglobulins, cytokines, and genes related to CD4+ T cell differentiation were determined by enzyme-linked immunosorbent assay (ELISA) and quantitative real-time PCR. Cytokine bioassay, mixed lymphocytes reaction and cell viability assay were performed.
Results: Topical application of sophoricoside decreased the symptoms of AD-like allergic skin inflammation, including elevated hypertrophic scars with spongiotic epidermis, epidermal hyperplasia, hyperkeratosis, infiltration of immune, and mast cells, dermal thickness, amounts of immunoglobulins, and pro-inflammatory cytokines, and the mast cell population in the skin. Sophoricoside also decreased T cell antigen receptor (TCR)-mediated immune responses. In particular, sophoricoside suppressed the differentiation of na?ve CD4+ T cells into Th cell subsets, including Th1, Th2, and Th17, by inhibiting the expression of their subset-specific master transcription factors, leading to suppression of the expression and production of these cell subset-specific cytokines.
Conclusion: Sophoricoside can improve AD-like allergic skin diseases mainly by inhibiting pathogenic CD4+ T cell differentiation and immune responses.
Sophoricoside from Sophora japonica ameliorates allergic asthma by preventing mast cell activation and CD4+ T cell differentiation in ovalbumin-induced mice
Asthma is a chronic inflammatory lung disorder with continuously increasing prevalence worldwide. Novel strategies are needed to prevent or improve asthma. The aim of this study was to investigate the effects of sophoricoside from Sophora japonica on allergic asthma. The mature seeds of S. japonica contain a large amount of sophoricoside. Sophoricoside reduced allergic and asthmatic symptoms by suppressing airway inflammation and antibody-antigen reaction in mouse models. In particular, sophoricoside suppressed immune cell recruitment into the airway lumens of the lungs and production of pro-inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of ovalbumin (OVA)-induced mice. It also decreased the amounts of histamine and arachidonic acid metabolites released in OVA-induced mice and antibody-antigen stimulated mast cells. In addition, sophoricoside decreased differentiation of na?ve CD4+ T cells into T helper type 1 (Th1), Th2, and Th17 cells. Overall, we demonstrated that sophoricoside improved allergic asthma by suppressing mast cell activation and CD4+ T cell differentiation.
Sophoricoside is a selective LXRβ antagonist with potent therapeutic effects on hepatic steatosis of mice
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by the accumulation of triglycerides and associated with obesity, hyperlipidemia and insulin resistance. Currently, there is no therapy for NAFLD. Emerging evidences suggest that the inhibition of liver X receptor (LXR) activity may be a potential therapy for hepatic steatosis. Here, we identified that sophoricoside is a selective antagonist of LXRβ. Sophoricoside protected against obesity and glucose tolerance, and inhibited lipid accumulation in the liver of high-fat diet-induced obesity (DIO) mice and methionine and choline-deficient diet-induced nonalcoholic steatohepatitis mice. Furthermore, sophoricoside inhibited malondialdehyde, and increased superoxide dismutase and glutathione in the liver of the mice. In HepG2 cells, pretreatment with sophoricoside rescued GSH concentration decrease induced by H2 O2 treatment. Our data suggest that sophoricoside is a novel LXRβ selective antagonist and may improve glucose and lipid dysfunction, and attenuate lipid accumulation in the liver of DIO mice via anti-oxidant properties, which may be developed as a therapy for NAFLD.
Sophoricoside ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy
Aim: The study aims to evaluate protective effects of sophoricoside (Sop) on cardiac hypertrophy. Meanwhile, the potential and significance of Sop should be broadened and it should be considered as an attractive drug for the treatment of pathological cardiac hypertrophy and heart failure.
Methods: Using the phenylephrine (PE)-induced neonatal rat cardiomyocytes (NRCMs) enlargement model, the potent protection of Sop against cardiomyocytes enlargement was evaluated. The function of Sop was validated in mice received transverse aortic coarctation (TAC) or sham surgery. At 1 week after TAC surgery, mice were treated with Sop for the following 4 weeks, the hearts were harvested after echocardiography examination.
Results: Our study revealed that Sop significantly mitigated TAC-induced heart dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis. Mechanistically, Sop treatment induced a remarkable activation of AMPK/mTORC1-autophagy cascade following sustained hypertrophic stimulation. Importantly, the protective effect of Sop was largely abolished by the AMPKα inhibitor Compound C, suggesting an AMPK activation-dependent manner of Sop function on suppressing pathological cardiac hypertrophy.
Conclusion: Sop ameliorates cardiac hypertrophy by activating AMPK/mTORC1-mediated autophagy. Hence, Sop might be an attractive candidate for the treatment of pathological cardiac hypertrophy and heart failure.