Dehydrocorydaline nitrate
Dehydrocorydaline has anti-inflammatory activity, it has antinociceptive effects in mouse models of inflammatory pain, the effects involve the opioid receptor and inflammatory cytokines. Dehydrocorydaline can inhibit elevated mitochondrial membrane potential in lipopolysaccharide-stimulated macrophages.Dehydrocorydaline not only inhibits antibody-mediated allergic reactions but also influences cell-mediated allergic reactions, and the inhibitory effect of Corydalis Tuber on allergic reactions may be partially attributed to dehydrocorydaline.
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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
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Int. Immunopharmacol., 2011, 11(9):1362-7.
Dehydrocorydaline inhibits elevated mitochondrial membrane potential in lipopolysaccharide-stimulated macrophages.[Pubmed:
21575743 ]
Activated macrophages play a critical role in the pathogenesis of numerous diseases by producing pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6. While the mechanisms of bacterial component recognition and signal transduction have been well investigated, viability regulation in activated macrophages remains unclear.
METHODS AND RESULTS:
We screened herbal ingredients to find an agent that reduces the viability of lipopolysaccharide (LPS)-stimulated macrophages and observed that dehydrocorydaline, a component of Corydalis yanhusuo, reduced the viability of macrophage-derived RAW264.7 cells and primary macrophages in the presence of LPS. Dehydrocorydaline inhibited the elevation of mitochondrial membrane potential and induced ATP depletion in LPS-stimulated macrophages but neither affected basal mitochondrial membrane potential nor ATP content in non-stimulated macrophages. Dehydrocorydaline also prevented increased concentrations of IL-1β and IL-6 in culture media of LPS-stimulated macrophages.
CONCLUSIONS:
Mode of dehydrocorydaline action indicates that elevated mitochondrial membrane potential may be a novel target to specifically reduce viability and suppress cytokine production in LPS-stimulated macrophages.
