2. Metabolic Enzyme/Protease Epigenetics Cell Cycle/DNA Damage MAPK/ERK Pathway Vitamin D Related/Nuclear Receptor Immunology/Inflammation
  3. Endogenous Metabolite Sirtuin JNK p38 MAPK PPAR AP-1
  4. Schizophyllan

Schizophyllan (SPG) is an orally active extracellular β-glucan produced by the fungus Schizophyllum commune. Schizophyllan improves mitochondrial function and protects against metabolic liver injury by activating the SIRT3 pathway. Schizophyllan inhibits osteoclastogenesis and promotes osteoblast differentiation by suppressing the phosphorylation of JNK/p38, as well as downregulating PGC1β/PPARγ, c-Fos and NFATc1. Recognized via Dectin-1, schizophyllan enables precise delivery of oligonucleotide drugs and antigens to antigen-presenting cells, thus holding great potential in the treatment of inflammatory diseases and vaccine development.

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Schizophyllan

Schizophyllan Chemical Structure

CAS No. : 9050-67-3

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Based on 1 publication(s) in Google Scholar

Schizophyllan Related Antibodies

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Human Endogenous Metabolite Microbial Metabolite

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Sirtuin SIRT1 SIRT2 SIRT3 SIRT6 SIRT5 SIRT7 SIRT4

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JNK1 JNK2 JNK3 JNK

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p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

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PPARα PPARβ/δ PPARγ PPAR PPARδ

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c-Fos FosB Fra1/FOSL1 Fra2/FOSL2 c-Jun

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Description

Schizophyllan (SPG) is an orally active extracellular β-glucan produced by the fungus Schizophyllum commune. Schizophyllan improves mitochondrial function and protects against metabolic liver injury by activating the SIRT3 pathway. Schizophyllan inhibits osteoclastogenesis and promotes osteoblast differentiation by suppressing the phosphorylation of JNK/p38, as well as downregulating PGC1β/PPARγ, c-Fos and NFATc1. Recognized via Dectin-1, schizophyllan enables precise delivery of oligonucleotide drugs and antigens to antigen-presenting cells, thus holding great potential in the treatment of inflammatory diseases and vaccine development[1][2][3].

In Vitro

Schizophyllan (5-200 μg/mL; 4-7 h) dose-dependently inhibits RANKL-induced osteoclast differentiation, TRAP activity, F-actin ring formation, and bone resorption in mouse bone marrow-derived macrophages. At the concentration of 200 μg/mL, it reduces the number of mature osteoclasts by approximately 95% and almost completely blocks bone resorption[1].
Schizophyllan (200 μg/mL; 0-4 d) downregulates the expression of RANKL-induced osteoclast differentiation marker genes, and inhibits key signaling pathways (JNK/p38 MAPK, PGC1β/PPARγ) and transcription factors (c-Fos, NFATc1) during osteoclastogenesis in mouse bone marrow-derived macrophages[1].
Schizophyllan (50-200 μg/mL; 1-6 d) dose-dependently inhibits osteoclast formation in a co-culture system of mouse bone marrow mononuclear cells and osteoblasts, and downregulates the expression of osteoclastogenic factors *Csf1* and *Tnfsf11* in mouse calvarial osteoblasts at the concentration of 200 μg/mL[1].
Schizophyllan (200 μg/mL; 7-24 d) slightly enhances mineralized nodule formation in mouse calvarial osteoblasts and upregulates the expression of osteoblast differentiation marker genes and transcription factors[1].
Schizophyllan (30 μg/mL) specifically binds to soluble recombinant mouse Dectin-1 protein, among which dA60 (S)/SPG exhibits the strongest binding activity[2].
Schizophyllan specifically hybridizes with target TNF-α sense RNA in vitro and does not dissociate from SPG[2].
Schizophyllan delivers the OVA257-264 peptide to murine peritoneal macrophages, and its antigen-presenting efficacy is comparable to that of the free conjugate[2].
Schizophyllan (0-24 h) is preferentially taken up by mouse RAW264 macrophages, and the uptake amount increases continuously within 24 h[2].
Schizophyllan (100 μg/mL; 1-2 d) regulates the acetylation level and expression of SOD2 in primary hepatocytes from SOD2−/− mice, and reduces mitochondrial ROS production in primary hepatocytes from wild-type mice in a SIRT3-dependent manner[3].

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

Schizophyllan Related Antibodies
In Vivo

Schizophyllan (25 mg/mouse; s.c.; daily; 9 days) significantly inhibits LPS (HY-D1056)-induced osteoclast formation and bone erosion in male ICR mice, reducing TRAP-positive osteoclast area by ~40% and osteoclast counts by ~36% compared to LPS-only treated animals[1].
Schizophyllan (100 mg/kg; p.o.; daily; 4-8 weeks) induces SIRT3 expression in mouse liver and adipose tissue, activates SOD2 via deacetylation, and improves hepatic mitochondrial function in a SIRT3-dependent manner[3].
Schizophyllan (100 mg/kg; p.o.; daily; 4-8 weeks) induces SIRT3-dependent deacetylation and activation of SDHA in mouse brown adipose tissue[3].
Schizophyllan (100 mg/kg; p.o.; daily; 6 weeks) reduces chronic ethanol-induced liver damage in wild-type mice via activation of the SIRT3-SOD2 pathway, restoring liver function and morphology[3].
Schizophyllan (100 mg/kg; p.o.; daily; 20 weeks) reduces CLA-induced metabolic adverse effects in wild-type mice via activation of the SIRT3-SDHA pathway, restoring tissue weights and serum chemistry markers[3].

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

Animal Model: ICR mice (5-week-old, male)[1]
Dosage: 25 mg/mouse
Administration: s.c.; daily; 9 days
Result: Reduced TRAP-positive osteoclast area to ~60% relative to LPS-only group (~100%).
Decreased eroded surface per bone surface (ES/BS) from ~30% to ~25% relative to LPS-only group.
Lowered osteoclast counts from ~28 to ~18 per field relative to LPS-only group.
Did not significantly alter TRAP-positive area, ES/BS, or osteoclast counts relative to PBS controls when administered alone.
Animal Model: C57BL/6J; SIRT3−/− (B6.129S6(Cg)Sirt3tm1.1Fwa/J); SOD2−/− (B6.129S7-Sod2tm1Leb/J) (female, 6 weeks old)[3]
Dosage: 100 mg/kg
Administration: p.o.; daily; 4 to 8 weeks
Result: Markedly induced SIRT3 expression in liver and brown adipose tissue, with peak mRNA and protein expression at 4-6 weeks.
Reduced SOD2 acetylation (K68 and K122 sites) in liver of wild-type mice.
Increased SOD2 enzyme activity to ~5 relative units/mg protein by 8 weeks in wild-type mice.
Increased hepatic oxygen consumption rate (including basal respiration and maximal respiratory capacity) in wild-type mice.
Reduced mitochondrial ROS production in wild-type mice.
Abrogated all above effects in SIRT3−/− mice.
Animal Model: C57BL/6J; SIRT3−/− (B6.129S6(Cg)Sirt3tm1.1Fwa/J); SDHA−/− (B6N(Cg)-Sdhatm2b(KOMP)Wtsi/2J) (female, 6 weeks old)[3]
Dosage: 100 mg/kg
Administration: p.o.; daily; 4 to 8 weeks
Result: Reduced SDHA acetylation in brown adipose tissue of wild-type mice.
Increased SDHA enzyme activity to ~5 relative units/mg protein by 8 weeks in wild-type mice.
Abrogated all above effects in SIRT3−/− and SDHA−/− mice.
Animal Model: C57BL/6J; SIRT3−/− (B6.129S6(Cg)Sirt3tm1.1Fwa/J) (female, 6 weeks old, alcohol-induced liver damage model)[3]
Dosage: 100 mg/kg
Administration: p.o.; daily; 6 weeks
Result: Reduced SOD2 acetylation in liver of wild-type mice.
Increased SOD2 enzyme activity in wild-type mice.
Reduced mitochondrial ROS production in wild-type mice.
Reduced blood acetaldehyde and ethanol levels in wild-type mice.
Restored final body weight to 21.94 g in wild-type mice.
Restored liver weight to 0.86 g in wild-type mice.
Reduced histologic liver damage in wild-type mice.
Abrogated all above protective effects in SIRT3−/− mice.
Animal Model: C57BL/6J; SIRT3−/− (B6.129S6(Cg)Sirt3tm1.1Fwa/J); SDHA−/− (B6N(Cg)-Sdhatm2b(KOMP)Wtsi/2J) (female, 6 weeks old)[3]
Dosage: 20 mg/kg; 100 mg/kg
Administration: p.o.; daily; 20 weeks
Result: Reduced SDHA acetylation in brown adipose tissue of wild-type mice at 100 mg/kg.
Increased SDHA enzyme activity in wild-type mice at 100 mg/kg.
Abrogated all above protective effects in SIRT3−/− and SDHA−/− mice.
CAS No.
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Solid

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White to off-white

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[Schizophyllan]
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In solvent -80°C 6 months
-20°C 1 month
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H2O : 1.82 mg/mL (ultrasonic and warming and adjust pH to 12 with 1 M NaOH and heat to 60°C)

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Keywords:

Schizophyllan9050-67-3SPGEndogenous MetaboliteSirtuinJNKp38 MAPKPPARAP-1c-Jun N-terminal kinasePeroxisome proliferator-activated receptorsActivator Protein 1osteoclastogenesisNFATc1c-FosPPARγIκBαSIRT3Dectin-1PGC1βp38Inhibitorinhibitorinhibit

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