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| Targets |
AMP-activated protein kinase (AMPK, activator) [3]
NF-κB signaling pathway (inhibitor) [1][2] MAPK signaling pathway (ERK1/2, JNK, p38; inhibitor) [1][2] HMGB1-mediated proinflammatory pathway (inhibitor) [2] |
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| ln Vitro |
In human umbilical vein endothelial cells (HUVECs) stimulated with TNF-α (10 ng/mL), Kaempferol 3-O-sophoroside (10, 30, 50 μM) dose-dependently inhibited the expression of proinflammatory mediators: IL-6 and IL-8 mRNA levels were reduced by 32%-68% and 28%-65%, respectively; VCAM-1 and ICAM-1 protein levels were decreased by 25%-58% and 22%-53% at 50 μM. It suppressed NF-κB activation by inhibiting p65 nuclear translocation and IκBα phosphorylation, and downregulated the phosphorylation of ERK1/2, JNK, and p38 MAPK. MTT assay showed no significant cytotoxicity at concentrations up to 50 μM. [1]
In HMGB1-stimulated RAW264.7 macrophages (100 ng/mL HMGB1), Kaempferol 3-O-sophoroside (10, 30, 50 μM) concentration-dependently reduced the production of NO (inhibition rate 29%-72%) and PGE₂ (inhibition rate 24%-68%) at 50 μM. It also decreased TNF-α, IL-6, and IL-1β mRNA and protein levels (by 35%-75% for mRNA, 30%-70% for protein) by inhibiting HMGB1-induced NF-κB p65 nuclear translocation and IκBα degradation, as well as MAPK pathway activation. No cytotoxicity was observed at concentrations ≤50 μM. [2] In LPS-stimulated BV2 microglial cells (1 μg/mL LPS), Kaempferol 3-O-sophoroside (1, 5, 10 μM) dose-dependently activated AMPKα1/2 phosphorylation (p-AMPKα levels increased by 1.8-3.2 folds) and inhibited the expression of proinflammatory cytokines (TNF-α, IL-6, IL-1β) and chemokines (CCL2, CXCL10) without affecting cell viability. [3] |
| ln Vivo |
In C57BL/6J mice subjected to chronic unpredictable mild stress (CUMS)-induced depressive-like behavior, oral administration of Kaempferol 3-O-sophoroside (10, 20, 40 mg/kg, once daily for 21 consecutive days) dose-dependently improved depressive phenotypes: The immobility time in the forced swim test (FST) was reduced by 28% (10 mg/kg), 42% (20 mg/kg), and 56% (40 mg/kg); the immobility time in the tail suspension test (TST) was decreased by 25% (10 mg/kg), 38% (20 mg/kg), and 51% (40 mg/kg); sucrose preference in the sucrose preference test (SPT) was increased by 18% (10 mg/kg), 29% (20 mg/kg), and 41% (40 mg/kg) compared to the CUMS control group. [3]
Mechanistic analysis in mouse hippocampal tissues showed that Kaempferol 3-O-sophoroside (40 mg/kg) activated AMPK signaling (p-AMPKα levels increased by 2.8 folds), reduced the expression of proinflammatory mediators (TNF-α, IL-6, iNOS, COX-2) by 45%-62%, and upregulated the expression of synaptic plasticity-related proteins (BDNF, PSD95) by 1.9-2.5 folds. [3] No significant adverse effects were observed: Mouse body weight, organ coefficients (liver, kidney, heart, lung, spleen), and serum biochemical parameters (ALT, AST, BUN, creatinine) were not significantly different from the normal control group. [3] |
| Enzyme Assay |
AMPK phosphorylation assay (Western blot-based): BV2 microglial cells or mouse hippocampal tissue lysates were prepared, and proteins were separated by SDS-PAGE, transferred to membranes, and probed with antibodies against phosphorylated AMPKα (p-AMPKα) and total AMPKα. The ratio of p-AMPKα to total AMPKα was quantified to assess AMPK activation. [3]
NF-κB activity assay (nuclear translocation detection): HUVECs or RAW264.7 cells were fixed, permeabilized, and incubated with anti-NF-κB p65 primary antibody and fluorescent secondary antibody. Nuclei were stained with DAPI, and the nuclear localization of p65 was observed under a confocal microscope to evaluate NF-κB activation. [1][2] NO production assay: RAW264.7 cells were treated with Kaempferol 3-O-sophoroside and HMGB1, and the culture supernatant was collected. NO levels were determined using a Griess reagent-based assay by measuring absorbance at 540 nm and comparing with a sodium nitrite standard curve. [2] PGE₂ production assay: RAW264.7 cell supernatants were analyzed for PGE₂ concentration using a competitive ELISA kit according to the protocol, with absorbance measured at the specified wavelength to quantify PGE₂ levels. [2] |
| Cell Assay |
HUVECs inflammatory response assay: HUVECs were seeded in 6-well plates and cultured to confluence, then serum-starved for 12 hours. Cells were pre-treated with Kaempferol 3-O-sophoroside (10, 30, 50 μM) for 1 hour, followed by stimulation with TNF-α (10 ng/mL) for 6 hours (for mRNA detection) or 12 hours (for protein detection). Total RNA was extracted for qPCR to measure IL-6, IL-8, VCAM-1, and ICAM-1 mRNA levels; total proteins were extracted for Western blot to detect VCAM-1, ICAM-1, p-p65, p-IκBα, p-ERK1/2, p-JNK, and p-p38 levels. MTT assay was performed to assess cell viability. [1]
RAW264.7 macrophage inflammatory response assay: RAW264.7 cells were seeded in 6-well plates and pre-treated with Kaempferol 3-O-sophoroside (10, 30, 50 μM) for 1 hour, then stimulated with HMGB1 (100 ng/mL) for 24 hours. Culture supernatants were collected for NO and PGE₂ detection; total RNA and proteins were extracted for qPCR and Western blot analysis of TNF-α, IL-6, IL-1β, p-p65, and p-IκBα. [2] BV2 microglial cell assay: BV2 cells were seeded in 6-well plates and pre-treated with Kaempferol 3-O-sophoroside (1, 5, 10 μM) for 1 hour, then stimulated with LPS (1 μg/mL) for 24 hours. Western blot was used to detect p-AMPKα and total AMPKα; qPCR was performed to measure TNF-α, IL-6, IL-1β, CCL2, and CXCL10 mRNA levels. [3] |
| Animal Protocol |
CUMS-induced depressive-like behavior mouse model [3]: Male C57BL/6J mice (6-8 weeks old) were randomly divided into 5 groups: normal control group, CUMS control group, Kaempferol 3-O-sophoroside low-dose group (10 mg/kg), middle-dose group (20 mg/kg), and high-dose group (40 mg/kg). The CUMS model was established by exposing mice to various mild stressors (e.g., food/water deprivation, cage tilting, cold stress) for 21 consecutive days. Kaempferol 3-O-sophoroside was dissolved in 0.5% carboxymethylcellulose sodium and administered via oral gavage once daily for 21 days (concurrently with CUMS induction). Behavioral tests (FST, TST, SPT) were performed on days 19-21. After sacrifice, hippocampal tissues were collected for Western blot (p-AMPKα, BDNF, PSD95) and qPCR (inflammatory cytokines) analysis; major organs (liver, kidney, heart, lung, spleen) were weighed to calculate organ coefficients; serum was collected for biochemical parameter detection. [3]
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| Toxicity/Toxicokinetics |
In vitro cytotoxicity: At concentrations up to 50 μM (HUVECs/RAW264.7) or 10 μM (BV2), kaempferol-3-O-sophoroside did not show significant cytotoxicity to HUVECs, RAW264.7 macrophages, or BV2 microglia. MTT assay results showed that cell viability was higher than 85% of the control group [1][2][3]. In vivo toxicity: After oral administration of kaempferol-3-O-sophoroside (10-40 mg/kg, 21 days) to C57BL/6J mice, there were no significant changes in body weight, food intake, organ coefficients (liver, kidney, heart, lung, spleen), or serum biochemical indicators (ALT, AST, BUN, creatinine). Histopathological examination of major organs did not reveal significant toxic lesions. [3]
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| References |
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| Additional Infomation |
Kaempferol 3-O-β-D-glucosyl-(1->2)-β-D-glucosinolate is a sophoroside composed of kaempferol linked to the 3 position of β-D-sophosyl residues via a glycosidic bond. It is a plant metabolite belonging to the trihydroxyflavones and sophorosides. Sophoroflavonoid glycosides have been reported to be found in horsetail, soybean and other organisms with relevant data. Kaempferol 3-O-sophosinolate is a natural flavonoid glycoside that can be isolated from medicinal plants such as Sophora flavescens. [4] (Note: Reference [4] mentions this plant, but focuses on other flavonoid compounds; the plant source of this compound is inferred from the extract) [1][2][3] Its anti-inflammatory mechanism involves inhibiting the NF-κB and MAPK signaling pathways, thereby reducing the production of pro-inflammatory cytokines and mediators (IL-6, IL-8, TNF-α, NO, PGE₂) in endothelial cells, macrophages and microglia. [1][2]
The antidepressant-like effect of kaempferol-3-O-sophoroside is mediated by activation of the AMPK signaling pathway in the hippocampus, which downregulates neuroinflammation and enhances synaptic plasticity (by upregulating BDNF and PSD95), thereby improving depressive-like behavior induced by chronic unpredictable stress (CUMS) in mice. [3] This compound exhibits good safety both in vitro and in vivo, with no significant toxicity observed at therapeutic concentrations/doses, supporting its potential as a lead compound for anti-inflammatory and antidepressant drugs. [1][2][3] |
| Molecular Formula |
C27H30O16
|
|---|---|
| Molecular Weight |
610.5175
|
| Exact Mass |
610.153
|
| CAS # |
19895-95-5
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| PubChem CID |
5282155
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| Appearance |
Off-white to light yellow solid powder
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| Density |
1.8±0.1 g/cm3
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| Boiling Point |
995.0±65.0 °C at 760 mmHg
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| Melting Point |
194-198℃
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| Flash Point |
329.3±27.8 °C
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| Vapour Pressure |
0.0±0.3 mmHg at 25°C
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| Index of Refraction |
1.764
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| LogP |
-0.58
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| Hydrogen Bond Donor Count |
10
|
| Hydrogen Bond Acceptor Count |
16
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
43
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| Complexity |
1000
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| Defined Atom Stereocenter Count |
10
|
| SMILES |
C1=CC(=CC=C1C2=C(C(=O)C3=C(C=C(C=C3O2)O)O)O[C@H]4[C@@H]([C@H]([C@@H]([C@H](O4)CO)O)O)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O)O
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| InChi Key |
LKZDFKLGDGSGEO-UJECXLDQSA-N
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| InChi Code |
InChI=1S/C27H30O16/c28-7-14-17(33)20(36)22(38)26(40-14)43-25-21(37)18(34)15(8-29)41-27(25)42-24-19(35)16-12(32)5-11(31)6-13(16)39-23(24)9-1-3-10(30)4-2-9/h1-6,14-15,17-18,20-22,25-34,36-38H,7-8H2/t14-,15-,17-,18-,20+,21+,22-,25-,26+,27+/m1/s1
|
| Chemical Name |
3-[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]oxy-5,7-dihydroxy-2-(4-hydroxyphenyl)chromen-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 Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| 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 (~163.79 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.09 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 (4.09 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 (4.09 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 | 1.6379 mL | 8.1897 mL | 16.3795 mL | |
| 5 mM | 0.3276 mL | 1.6379 mL | 3.2759 mL | |
| 10 mM | 0.1638 mL | 0.8190 mL | 1.6379 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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