2. Immunology/Inflammation NF-κB Cytoskeleton TGF-beta/Smad Metabolic Enzyme/Protease Apoptosis
  3. Toll-like Receptor (TLR) NF-κB Collagen Interleukin Related Cadherin NOD-like Receptor (NLR) TGF-β Receptor FXR Apoptosis
  4. Ligusticum cycloprolactam

Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease.

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Ligusticum cycloprolactam

Ligusticum cycloprolactam Chemical Structure

CAS No. : 2283387-37-9

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Ligusticum cycloprolactam Related Antibodies

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Description

Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease[1][2][3][4].

IC50 & Target[1]

TLR4

 

IL-6

 

IL-1b

 

IL-1β

 

NLRP3

 

In Vitro

Ligusticum cycloprolactam (LIGc) (2.5-10 μM; 2 h) dose-dependently suppresses LPS (HY-D1056)-induced pro-inflammatory mediator (NO, TNF-α, IL-1β) production and promotes anti-inflammatory cytokine (IL-4, IL-10) secretion in RAW264.7 mouse macrophages[1].
Ligusticum cycloprolactam (2.5-10 μM; 2 h) dose-dependently reduces LPS-induced pro-inflammatory protein (CD86, iNOS, COX-2) expression and increases anti-inflammatory protein (CD206) expression in RAW264.7 mouse macrophages[1].
Ligusticum cycloprolactam (10 μM; 2 h) inhibits LPS-induced pro-inflammatory gene (cd86, Nos2) expression in RAW264.7 mouse macrophages[1].
Ligusticum cycloprolactam (LIGc) (10 μM; 2 h) reduces LPS-induced pro-inflammatory CD86 marker expression in primary mouse microglia[1].
Ligusticum cycloprolactam (10 μM; 2 h) modulates the transcriptional profile of LPS-stimulated RAW264.7 mouse macrophages, with significant downregulation of the pro-inflammatory Fpr1 gene and enrichment of anti-inflammatory signaling pathways[1].
Ligusticum cycloprolactam (10 μM; 2 h) inhibits LPS-induced FPR1 protein expression in RAW264.7 mouse macrophages[1].
Ligusticum cycloprolactam (10 μM; 2 h) inhibits LPS-induced NLRP3 protein expression in RAW264.7 mouse macrophages and primary mouse microglia[1].
Ligusticum cycloprolactam (10 μM; 2 h) exerts anti-inflammatory effects in LPS-stimulated RAW264.7 mouse macrophages and primary mouse microglia by downregulating the FPR1/NLRP3 signaling axis, as FPR1 overexpression reverses these effects[1].
Ligusticum cycloprolactam (20-80 μM; 36 h) ameliorates uric acid (HY-B2130)-induced injury in NRK-52E cells by suppressing the TLR4/NF-κB signaling pathway, reducing inflammatory and fibrotic responses[2].
Ligusticum cycloprolactam (2.5-40 μM; 24 h) has no cytotoxic effect on BV2 microglia cells at concentrations up to 20 μM for 24 h, but reduces cell viability at 40 μM[3].
Ligusticum cycloprolactam (5-20 μM; 1 h) dose-dependently reduces LPS-induced NO production in BV2 microglia cells, with the strongest inhibition at 10 μM[3].
Ligusticum cycloprolactam (5-20 μM; 1 h) dose-dependently reduces LPS-induced TNF-α and IL-1β secretion in BV2 microglia cells[3].
Ligusticum cycloprolactam (10 μM; 1 h) inhibits LPS-induced activation of the NF-κB pathway in BV2 microglia cells by reducing phosphorylation of IκBα, IKKα+β, and NF-κB p65[3].
Ligusticum cycloprolactam (10 μM; 1 h) protects HT22 hippocampal neuron cells from neurotoxicity induced by conditioned medium from LPS-activated BV2 microglia cells, restoring HT22 cell viability[3].
Ligusticum cycloprolactam (10 μM; 1 h) attenuates LPS-activated BV2 microglia-induced apoptosis in HT22 hippocampal neuron cells by restoring the Bcl2/Bax ratio and reducing BID and CytC expression[3].
Ligusticum cycloprolactam (LIGc) directly binds to purified FXR protein in a cell-free molecular docking assay[4].

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

Ligusticum cycloprolactam Related Antibodies

ELISA Assay[1]

Cell Line: LPS-stimulated RAW264.7 mouse macrophages
Concentration: 2.5; 5; 10 μM
Incubation Time: 2 h
Result: Dose-dependently inhibited LPS-induced production of NO, TNF-α, and IL-1β.
Enhanced secretion of IL-4 and IL-10, with optimal effects observed at 10 μM.
All changes were statistically significant compared to the LPS-only group.

Western Blot Analysis[1]

Cell Line: LPS-stimulated RAW264.7 mouse macrophages
Concentration: 2.5; 5; 10 μM
Incubation Time: 2 h
Result: Dose-dependently attenuated LPS-induced upregulation of CD86, iNOS, and COX-2 protein expression, while increasing CD206 protein expression, with significant differences compared to the LPS-only group at all tested concentrations.

Western Blot Analysis[1]

Cell Line: LPS-stimulated RAW264.7 mouse macrophages
Concentration: 10 μM (2 h pretreatment); 100 ng/mL LPS (12 h co-treatment)
Incubation Time: 2 h (pretreatment); 12 h (co-treatment)
Result: Significantly suppressed LPS-induced FPR1 protein expression, compared to the LPS-only group.

Western Blot Analysis[2]

Cell Line: NRK-52E cells
Concentration: 20; 40; 80 μM
Incubation Time: 36 h
Result: Effectively reversed the uric acid-induced
upregulation of transcription levels for inflammatory and fibrotic markers such as Nlrp3, IL-1b, Fn1 and Tgfb1.
Decreased the levels of KIM-1, NLRP3, IL-1β, VCAM1, FN and α-SMA proteins while enhancing E-cadherin protein expres-
sion.

ELISA Assay[3]

Cell Line: LPS-stimulated mouse BV2 microglia cells
Concentration: 5; 10; 20 μM
Incubation Time: 1 h
Result: Significantly attenuated LPS-induced increase in TNF-α and IL-1β secretion at 5, 10, and 20 μM.
Exhibited the most potent inhibitory effect on both cytokines at 10 μM.

Cell Viability Assay[3]

Cell Line: BV2 microglia cells
Concentration: 2.5; 5; 10; 20; 40 μM
Incubation Time: 24 h
Result: Showed cytotoxic effect on BV2 microglia cells at concentrations up to 20 μM.
Reduces cell viability at 40 μM.
In Vivo

Ligusticum cycloprolactam (LIGc) (20 and 60 mg/kg; p.o.; daily; 4 days) attenuates neuroinflammation in LPS-induced neuroinflammatory mice by suppressing pro-inflammatory microglia/macrophage activation and modulating the FPR1/NLRP3 signaling axis[1].
Ligusticum cycloprolactam (20 and 60 mg/kg; i.g.; at 1, 24, and 48 hours post-I/R) dose-dependently reduces cerebral infarction volume and improves neurological function in tMCAO mice[1].
Ligusticum cycloprolactam (20-80 mg/kg; i.g.; daily; 3 weeks) ameliorates hyperuricemic nephropathy in mice by reducing uric acid levels, renal inflammation, and fibrosis via inhibition of the TLR4/NF-κB pathway[2].

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

Animal Model: Adult male Kunming mice (8-10 weeks old, 24 g)[1]
Dosage: 20; 60 mg/kg
Administration: p.o.; daily; 4 days
Result: Improved LPS-induced alterations in open field metrics including increased distance covered, distance in center, time in center, and activity time, alongside decreased time in corner and rest time.
Reduced the number of Iba1+CD86+ pro-inflammatory microglia/macrophages in the cerebral cortex.
Suppressed cerebral cortex levels of pro-inflammatory markers TNF-α, IL-1β, CD86, iNOS, and COX-2, while increasing anti-inflammatory markers IL-4, IL-10, and CD206 at 20 mg/kg dose.
Produced similar, more pronounced effects at 60 mg/kg dose, including significant suppression of FPR1 and NLRP3 protein expression in the cerebral cortex.
Animal Model: Adult male Kunming mice (8-10 weeks old, 24 g) tMCAO model[1]
Dosage: 20; 60 mg/kg
Administration: i.g.; at 1, 24, and 48 hours post-I/R
Result: Reduced cerebral infarction volume in a dose-dependent manner, with the 60 mg/kg dose producing a larger reduction.
Improved neurological function significantly, as shown by lower Longa scores, reduced rightward turning tendency in the corner test, and increased use of the affected forelimb in the cylinder test.
Decreased the number of Iba1+CD86+ pro-inflammatory microglia/macrophages in the infarct-surrounding cerebral cortex, suppressed pro-inflammatory markers TNF-α, IL-1β, CD86, iNOS, and COX-2, and increased anti-inflammatory markers IL-4, IL-10, and CD206.
Significantly reduced FPR1 and NLRP3 protein expression in the cerebral cortex at 60 mg/kg dose.
Animal Model: Male C57BL/6J ( 8-week-old) with hyperuricemic nephropathy induced by hypoxanthine and potassium oxonate[2]
Dosage: 20, 40, 80 mg/kg
Administration: i.g.; daily; 3 weeks
Result: Reduced elevated serum uric acid levels and liver xanthine oxidase (XOD) activity.
Lowered kidney index, serum creatinine, blood urea nitrogen, and 24-hour albuminuria.
Ameliorated renal histological damage.
Dose-dependently reduced macrophage infiltration (F4/80-positive staining) and downregulated mRNA/protein expression of inflammatory markers (F4/80, Icam-1, IL-6, Ccl2, Nlrp3, IL-1b, MCP-1, NLRP3, IL-1β).
Decreased renal collagen deposition and downregulated fibrosis markers (Fn1, Col4a1, Tgfb1, Timp1, FN, α-SMA) while increasing E-cadherin.
Reversed dysregulation of renal uric acid transporters (upregulated Abcg2, Oat3, Oct2 mRNA and OAT1 protein.
Downregulated Glut9 mRNA and URAT1, GLUT9 protein.
Inhibited TLR4/NF-κB signaling.
Molecular Weight

247.33

Formula

C15H21NO2
CAS No.
SMILES

O=C1C2=C(C(N1C3CC3)(CCCC)O)CCC=C2
Structure Classification
Initial Source
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Storage

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Purity & Documentation
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Ligusticum cycloprolactam Related Classifications

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Keywords:

Ligusticum cycloprolactam2283387-37-9Toll-like Receptor (TLR)NF-κBCollagenInterleukin RelatedCadherinNOD-like Receptor (NLR)TGF-β ReceptorFXRApoptosisNuclear factor-κBNuclear factor-kappaBILTransforming growth factor beta receptorsNR1H4TGF-β signalingNLRP3 inflammasomeTLR4/NF-κBprimary mouse microgliaFPR1BV2 microglia cellsNRK-52E cellsMAPKRAW264.7 mouse macrophagesInhibitorinhibitorinhibit

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