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> Leucrose [7158-70-5]

Leucrose [7158-70-5]

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Referência HY-123115-100mg

Tamanho : 100mg

Marca : MedChemExpress


Description

Leucrose (5-O-α-D-Glucopyranosyl-D-fructose) is an orally active Sucrose (HY-B1779) isomer naturally found in pollen and honey. Leucrose promotes phosphorylation of JAK1 and STAT6, reduces pro-inflammatory mediators and cytokinesas (TNFα, and IL-1β), increases M2 macrophage polarization and suppresses DSS (HY-116282C)-induced colitis. Leucrose suppresses hepatic triglyceride accumulation, improves fasting blood glucose levels, and regulates hepatic lipogenesis and fatty acid β-oxidation in high-fat diet-induced obese mice. Leucrose is slowly hydrolyzed into glucose and fructose by α-glucosidase and acts as as a sugar substitute in diet[1][2][3].

IC50 & Target[1]

JAK1

 

STAT6

 

IL-1β

 

In Vitro

Leucrose (24 h) does not alter RAW 264.7 macrophage cell viability relative to glucose treatment in DMEM containing IL4 (20 ng/mL) and total glucose
content (25 mM) partially substituted with leucrose, but upregulates M2 macrophage markers (CD163, Arg1) and increases JAK1/STAT6 phosphorylation[1].
Leucrose is hydrolyzed into
glucose and fructose by α-glucosidase in the small intestine and suppresses adipogenesis and down-regulates adipogenesis-related gene expression in 3T3-L1 adipocytes[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Leucrose Related Antibodies

Cell Viability Assay[1]

Cell Line: RAW 264.7 macrophage cells
Concentration: 25% substitution of 25 mM glucose content; 50% substitution of 25 mM glucose content
Incubation Time: 24 h
Result: Significantly exceeds levels in the non-treated control group across all treated groups.
Shows no significant difference between leucrose-treated groups (25% and 50% substitution) and the glucose-treated group.

Western Blot Analysis[1]

Cell Line: RAW 264.7 macrophage cells
Concentration: 25% substitution of 25 mM glucose content; 50% substitution of 25 mM glucose content
Incubation Time: 24 h (with 20 ng/mL IL-4)
Result: Increases CD163 levels by 99.0% in the 50% leucrose substitution group compared to the high-glucose control group.
Increases Arg1 levels by 78.6% in the 50% leucrose substitution group compared to the high-glucose control group.
Significantly increases p-JAK1 levels in both the 25% and 50% leucrose substitution groups compared to the high-glucose control group.
Significantly increases p-STAT6 levels in both the 25% and 50% leucrose substitution groups compared to the high-glucose control group.
In Vivo

Leucrose (25-50% of total sucrose content replaced; p.o.; ad libitum in diet; continuously for 5 weeks) supplementation suppresses DSS (HY-116282C)-induced colitis in C57BL/6 mice, with the 50% replacement group reducing DAI AUC0-t by 37.3%, restoring colon length by 20.3%, and reducing colon tissue IL-1β mRNA levels by 81.1% relative to the DSS-only group, via regulation of inflammatory mediators and M2 macrophage polarization[1].
Leucrose (25-50% of total sucrose replaced; p.o.; ad libitum in diet; 12 weeks) improves fasting blood glucose levels, reduces hepatic triglyceride accumulation, downregulates hepatic lipogenesis-related genes, and upregulates hepatic β-oxidation-related genes in obese mice, with the 50% replacement showing greater potency for hepatic triglyceride reduction and β-oxidation gene activation[2].
Leucrose (25% indiet; p.o.; daily; 6 weeks) supports normal growth in weanling male SPF-Sprague-Dawley rats, with body weight gain, protein efficiency, and energy efficiency statistically equivalent to sucrose or corn starch controls[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6 (male, 5-week-old, 18-20 g, DSS-induced colitis model)[1]
Dosage: 25% of total sucrose content replaced with leucrose; 50% of total sucrose content replaced with leucrose
Administration: p.o.; ad libitum in diet; continuously for 5 weeks
Result: Attenuated DAI scores at day 19 by 59.2% (25% replacement) and 56.9% (50% replacement) compared to the DSS-only group.
Suppressed DAI area under the curve (AUC) scores by 25.4% (25% replacement) and 37.3% (50% replacement) compared to the DSS-only group.
Restored colon length by 12.6% (25% replacement) and 20.3% (50% replacement) compared to the DSS-only group.
Reduced myeloperoxidase (MPO) activity by 30.4% (25% replacement) and 31.9% (50% replacement) compared to the DSS-only group.
Reduced colon tissue iNOS protein levels by 89.3% (50% replacement) and COX2 protein levels by 84.0% (50% replacement) compared to the DSS-only group.
Down-regulated colon tissue mRNA levels of MCP-1, TNFα, and IL-1β by 44.7%, 34.7%, and 81.1% respectively in the 50% replacement group compared to the DSS-only group.
Reduced plasma IL-1β concentrations by 36.9% (25% replacement) and 34.4% (50% replacement) compared to the DSS-only group.
Significantly reduced colon tissue F4/80-positive macrophage infiltration compared to the DSS-only group in both leucrose groups.
Significantly increased colon tissue mRNA levels of M2 polarization markers Arg1 and Ym1 in both leucrose groups, and CD206 in the 50% replacement group only, compared to the DSS-only group.
Animal Model: C57BL/6 (5-week-old male, 18-20 g, high-fat diet-induced obesity model)[2]
Dosage: 25% of total sucrose replaced with leucrose; 50% of total sucrose replaced with leucrose
Administration: p.o.; ad libitum in diet; 12 weeks
Result: Reduced fasting blood glucose levels to 141 mg/dL (L25 group) and 133 mg/dL (L50 group), compared to HFD control's 184 mg/dL.
Reduced hepatic triglyceride content to 70 mg/g in L50 group compared to HFD control; L25 group showed non-significant reduction.
Downregulated peroxisome proliferator-activated receptor γ (Pparg) in L25 and L50 groups; downregulated sterol regulatory element binding protein 1C (Srebf1) in both leucrose groups; fatty acid synthase (Fasn) showed non-significant downward trend.
Upregulated peroxisome proliferator-activated receptor α (Ppara) and acyl CoA oxidase (Acox1) in L50 group; upregulated carnitine palmitoyltransferase 1A (Cpt1a) in both L25 and L50 groups, reversing HFD-induced downregulation.
Masse moléculaire

342.30

Formule

C12H22O11
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

OCC([C@@H](O)[C@H](O)[C@@H](CO)O[C@H]1O[C@@H]([C@H]([C@@H]([C@H]1O)O)O)CO)=O
Livraison

Room temperature in continental US; may vary elsewhere.
Stockage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvant et solubilité
In Vitro: 

H2O : 70 mg/mL (204.50 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.9214 mL 14.6071 mL 29.2141 mL
5 mM 0.5843 mL 2.9214 mL 5.8428 mL
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* 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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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