Atractylenolide I Immunology & Inflammation related inhibitor

Cat.No.S8291

Atractylenolide I is the major sesquiterpenoid of the rhizome of A. macrocephala and shows a wide spectrum of pharmacological activities such as antiinflammatory, digestion promoting, and antioxidant effects.
Atractylenolide I Immunology & Inflammation related inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 230.30

Quality Control

Cell Culture, Treatment & Working Concentration

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HepG2 cells Function assay Transactivation of p53 in human HepG2 cells expressing MDM2 promoter by transient transfection reporter assay
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Chemical Information, Storage & Stability

Molecular Weight 230.30 Formula

C15H18O2

Storage (From the date of receipt)
CAS No. 73069-13-3 Download SDF Storage of Stock Solutions

Synonyms N/A Smiles CC1=C2CC3C(=C)CCCC3(C=C2OC1=O)C

Solubility

In vitro
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In vivo
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Mechanism of Action

In vitro
Atractylenolide I decreases the TNF-α level in LPS-stimulated peritoneal macrophages in a dosedependent manner, IC50=23.1 μM. It also inhibits NO production in LPS-activated peritoneal macrophages, IC50=41 μM. The IC50 of this compound for inhibiting the activity of iNOS is 67.3 μM. It shows no marked effects against 5-lipoxygenase (5-LOX) and cyclooxygenase (COX). This chemical is also reported previously to act on white blood cell membranes and TLR4 and its antiinflammatory activity is related to antagonizing TLR4 [1].
In vivo
Atractylenolide I has anti-inflammatory effects. The treatment of this compound significantly attenuates LPS-induced lung wet-to-dry weight ratio and MPO activity in LPS-induced acute lung injury mouse. It also significantly inhibits the production of TNF-α, IL-6, IL-1β, IL-13, and MIF production in bronchoalveolar lavage fluid (BALF), as well as neutrophils and macrophages in BALF, upregulates the production of IL-10 in BALF. This chemical protects mice acute lung injury induced by LPS via inhibition of TLR4 expression and NF-κB activation[2].
References

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