1. Esculentic acid has anti-inflammatory effect.
2. Esculentic acid has protective effects against LPS-induced endotoxic shock may be mediated, at least in part, by regulation the release of inflammatory cytokines and mediators, and protein expression of COX-2 in mice.
6,7-Dihydroxycoumarin(Esculetin) has various biological and pharmaceutical properties including anti-edema, anti-inflammatory, anti-tumour, hepatoprotective, anti-osteoarthritis and anti-rheumatoid arthritis effects. It inhibits lipoxygenases (LOs), p42/44 MAPK activation, PI3-kinase activation, as well as NF-kappaB and AP-1 activation, it exhibits competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)- alanine by mushroom, the IC50 value of is 43 microM.
Sinomenine shows neuroprotective, anti- rheumatoid arthritis, anti-inflammatory and immunosuppressive effects, it can attenuate 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice and the therapeutic mechanism may be related to the reduction of up-regulated colonic TNF-alpha and IFN-gamma production caused by TNBS. Sinomenine also provides a novel therapy to treat ICH induced brain injury. Sinomenine can prevent galactosamine (GalN)/lipopolysaccharide (LPS) -treated hepatic failure by suppressing TNF production and/or reactive oxygen generation.
Momordin Ic has hypoglycemic, anticancer, anti-allergic, anti-pruritogenic, hepatoprotective, antinociceptive and anti-inflammatory effects. It accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT(2), possibly 5-HT(2C) and/or 5-HT(2B) receptors, which, in turn, increases synthesis of prostaglandins. Momordin Ic induces apoptosis through oxidative stress-regulated mitochondrial dysfunction involving the MAPK and PI3K-mediated iNOS and HO-1 pathways.
Vitexicarpin has shown antitumor, cytotoxicity, anti-inflammatory, analgesic and immunoregulatory properties.Vitexicarpin can act as a novel angiogenesis inhibitor, it exerts good antiangiogenic effects by inhibiting vascular-endothelial-growth-factor-(VEGF-) induced endothelial cell proliferation, migration, and capillary-like tube formation on matrigel in a dose-dependent manner. It can significantly reduce vascular inflammation, through inhibition of ROS-NF-κB pathway in vascular endothelial cells.