Isomeranzin
Isomeranzin has anti-inflammatory activity, it suppresses inflammation by inhibiting M1 macrophage polarization through the p65, NF-κB and ERK pathway.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Molecules 2022, 27(3),1047.
Natural Product Sciences2024, 30(4):309-315.
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Int Immunopharmacol. 2016 Sep;38:175-85.
Isomeranzin suppresses inflammation by inhibiting M1 macrophage polarization through the NF-κB and ERK pathway.[Pubmed:
27285671 ]
Macrophage polarization plays an important role in inflammation. Regulation of the polarization has been reported to be effective therapeutics for various kinds of inflammatory diseases. The aims of the present study were to investigate the anti-inflammatory property of Isomeranzin isolating from Murraya exotica as well as potential molecular mechanisms.
METHODS AND RESULTS:
Results showed that Isomeranzin specifically reduced the M1 macrophage-associated pro-inflammatory cytokines through down-regulation of NF-κB and ERK signals. Immunoprecipitation and RNA silencing indicated suppression of Isomeranzin in NF-κB activation was relying on the decreasing of TRAF6 ubiquitination. In vivo studies showed Isomeranzin evidently inhibited LPS-induced sepsis for rising survival rate, improving tissue damage and lessening inflammatory cytokines. In accordance with in vitro studies, Isomeranzin significantly blocked expression of p-p65 and p-ERK in lung and liver tissues. Moreover, Isomeranzin ameliorated DSS and TNBS-induced colitis due to its anti-inflammatory effects.
CONCLUSIONS:
Taken together, Isomeranzin suppressed inflammatory diseases by controlling M1 macrophage polarization through the NF-κB and ERK pathway.
