Hecubine
Hecubine is a monoterpene indole alkaloid found in Ervatamia ocinalis. Hecubine activates TREM2 expression, reduces LPS (HY-D1056)-stimulated inammatory cytokines (TNF-α、IL-6、IL-1β) overexpression, as well as suppresses the levels of TLR4-, MyD88-, MAPK/PI3K/AKT- and NF-κB-related proteins. Hecubin also exhibits antioxidative effect, reduces ROS production and activates of the Nrf2/HO-1 pathway. Hecubine rescues LPS-induced behavioral deficits in zebrash larvae. Hecubine can be used for the research of neural inflammation-associated central nervous system diseases.
For research use only. We do not sell to patients.
- CAS No.: 62874-52-6
- Formula: C20H26N2O
- Molecular Weight:310.43
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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TREM-2 |
HO-1 |
IL-1β |
IL-6 |
Hecubine directly binds to purified TREM2 protein with a binding affinity of -7.07 ± 0.03 kcal/mol[1].
Hecubine (25 μM; 1 h) directly interacts with TREM2 in BV2 microglial cells, increasing the protein's thermal stability by shifting its Tm by 6.4 ± 0.7 °C[1].
Hecubine (0.7-50 μM; 1 h pretreatment, followed by 24 h LPS stimulation) inhibits LPS (HY-D1056)-induced NO production in BV2 microglial cells with an IC50 of ~6 μM, achieving 52.1%, 64.6%, and 73.8% inhibition at 6, 12, and 25 μM respectively[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by 24 h LPS stimulation) suppresses LPS-induced production of pro-inflammatory mediators (PGE2, TNF-α, IL-6, IL-1β) and restores IL-10 levels in BV2 microglial cells, with maximal effects at 25 μM including reducing PGE2 to 15.3% and IL-6 to <8.8% of LPS-treated levels[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation) upregulates TREM2 expression, downregulates TLR4/MyD88 signaling, inhibits MAPK/PI3K/AKT and NF-κB pathway activation, and reduces iNOS/COX-2 expression in LPS-stimulated BV2 microglial cells, with 25 μM Hecubine suppressing p38/AKT phosphorylation and NF-κB p65 nuclear translocation by ~45%, ~45.6%, and ~40.1% respectively[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation) inhibits LPS-induced ROS production in BV2 microglial cells in a dose-dependent manner[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation; or 1 h treatment alone) activates the Nrf2/HO-1 antioxidant pathway in BV2 microglial cells, with 25 μM Hecubine increasing Nrf2 and HO-1 expression by 4.45-fold and 8.69-fold respectively in LPS-stimulated cells, and increasing expression of both proteins in a dose-dependent manner in unstimulated cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:LPS-stimulated mouse BV2 microglial cells
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Concentration:6, 12, 25 μM
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Incubation Time:1 h pretreatment, followed by 24 h LPS stimulation
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Result:Reduced LPS-induced PGE2 production to 15.3% of the LPS-treated group at 25 μM.
Suppressed LPS-induced TNF-α, IL-6, and IL-1β secretion, with 25 μM decreasing IL-6 levels to <8.8% of the LPS-treated group.
Reversed the LPS-induced decrease in the anti-inflammatory cytokine IL-10 in a dose-dependent manner.
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Cell Line:LPS-stimulated mouse BV2 microglial cells
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Concentration:6, 12, 25 μM
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Incubation Time:1 h pretreatment, followed by LPS stimulation
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Result:Dose-dependently increased TREM2 protein expression.
Inhibited LPS-induced increases in TLR4, MyD88, iNOS, and COX-2 protein expression.
Suppressed LPS-induced phosphorylation of p38, JNK, ERK 1/2, AKT, IKKα/β, IκBα, and NF-κB p65.
At 25 μM, inhibited p38 and AKT phosphorylation to ~55% and ~54.4% of LPS-treated levels respectively, and reduced LPS-induced NF-κB p65 nuclear translocation to ~59.9% of LPS-treated levels.
Increased Nrf2 and HO-1 protein expression by 4.45-fold and 8.69-fold at 25 μM respectively.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Zebrash larvae wild-type (4 days post-fertilization larvae)[1]
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Dosage:6 μM; 12 μM; 25 μM
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Administration:continuous exposure; 24 hours prior to LPS injection
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Result:Significantly increased the total swimming distance of LPS-injected larvae, reversing LPS-induced behavioral deficits.
Suppressed LPS-induced NO production and reduced LPS-induced Iba1 protein expression at 25 μM.
Dose-dependently inhibited LPS-induced increases in iNOS protein and mRNA expression, as well as IL-1β protein expression.
Reversed LPS-induced upregulation of TNF-α, IL-1β, and IL-6 mRNA expression.
Reduced LPS-induced ROS accumulation.
Increased TREM2, Nrf2 and HO-1 protein expression in LPS-injected larvae.
Chemical Information
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CAS No. 62874-52-6
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Molecular Weight 310.43
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Formula C20H26N2O
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SMILES
CC[C@@]12[C@@]3([H])[C@](C[N@](CCC4=C(N(C5=CC=CC=C54)C)CC2)C1)([H])O3
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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