Isopedicin
Isopedicin has anti-inflammatory functions, it inhibits the O(2)(*)(-) production in human neutrophils by an elevation of cellular cAMP and activation of PKA through its inhibition of cAMP-specific PDE.
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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.
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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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Free Radic Biol Med. 2009 Feb 15;46(4):520-8.
Potent inhibition of superoxide anion production in activated human neutrophils by isopedicin, a bioactive component of the Chinese medicinal herb Fissistigma oldhamii.[Pubmed:
19100830 ]
Fissistigma oldhamii is widely used in traditional Chinese medicine to treat rheumatoid arthritis. Activation of neutrophils is a key feature of inflammatory diseases. Herein, the anti-inflammatory functions of Isopedicin, a flavanone derived from F. oldhamii, and its underlying mechanisms were investigated in human neutrophils.
METHODS AND RESULTS:
Isopedicin potently and concentration-dependently inhibited superoxide anion (O(2)(*)(-)) production in formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP)-activated human neutrophils with an IC(50) value of 0.34+/-0.03 microM. Furthermore, Isopedicin displayed no superoxide-scavenging ability, and it failed to alter subcellular NADPH oxidase activity. The inhibitory effect of Isopedicin on O(2)(*)(-) production was reversed by protein kinase A (PKA) inhibitors. Moreover, Isopedicin increased cAMP formation and PKA activity in FMLP-activated human neutrophils, which occurred through the inhibition of phosphodiesterase (PDE) activity but not an increase in adenylate cyclase function. In addition, Isopedicin reduced FMLP-induced phosphorylation of extracellular regulated kinase and c-Jun N-terminal kinase, which was reversed by the PKA inhibitor. In contrast, Isopedicin failed to alter FMLP-induced phosphorylation of p38 mitogen-activated protein kinase and calcium mobilization.
CONCLUSIONS:
In summary, these results demonstrate that inhibition of O(2)(*)(-) production in human neutrophils by Isopedicin is associated with an elevation of cellular cAMP and activation of PKA through its inhibition of cAMP-specific PDE.
