Kukoamine B, as a constituent of Lycii Cortex, exhibits anti-acute inflammatory, anti-oxidant, and anti-diabetic characteristics.

Kukoamine B is a spermine alkaloid first isolated from a traditional Chinese herb?L. chinense?that inhibits both lipopolysaccharides (LPS) and oligodeoxynucleotides containing CpG motifs (CpG DNA).It is reported to inhibit proinflammatory signal transduction and cytokine expression induced by LPS and CpG DNA (Kds = 1.24 and 0.66 μM).1LPS and CpG DNA are two well-recognized pathogen-associated molecular patterns (PAMPs) that play a role in triggering sepsis, thus sepsis may be attenuated by simultaneously neutralizing LPS and CpG DNA.Kukoamine B inhibit proinflammatory signal transduction and cytokine expression induced by LPS and CpG DNA (Kds = 1.24 and 0.66 μM). LPS and CpG DNA are two well-recognized pathogen-associated molecular patterns (PAMPs) that play a role in triggering sepsis, thus sepsis may be attenuated by simultaneously neutralizing LPS and CpG DNA.

Kukoamine B(KB) had high affinities for LPS and CpG DNA. It neutralized LPS and CpG DNA and prevented them from interacting with mouse macrophages. KB selectively inhibited LPS- and CpG DNA-induced signal transduction and expression of pro-inflammatory mediators without interfering with signal pathways or cell viability in macrophages. KB protected mice challenged with heat-killed Escherichia coli, and reduced the circulatory levels of LPS and TNF-α[1].

The affinities of Kukoamine B for LPS and CpG DNA were assessed using biosensor technology.?Direct interaction of Kukoamine B with LPS and CpG DNA were evaluated using neutralization assays.?Selective inhibitory activities of Kukoamine B on pro-inflammatory signal transduction and cytokine expression induced by LPS and CpG DNA were analysed by cellular assays.?Protective effects of KB in a sepsis model in mice were elucidated by determining survival and circulatory LPS and tumour necrosis factor-alpha (TNF-α) concentrations.

DMSO: 30 mg/mL (56.53 mM), Sonication is recommended.