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.
1. Esculetin(6,7-Dihydroxycoumarin) is known to inhibit proliferation and induce apoptosis in several types of human cancer cells and is regarded as a promising chemotherapeutic agent; it inhibits cell growth and induces apoptosis by suppressing Sp1 in HN22 and HSC4 cells, suggesting it to be a potent anticancer drug candidate for oral cancer.
2. Esculetin blocks cell proliferation via the inhibition of an upstream effector of Ras and downstream events including p42/44 MAPK activation, PI 3-kinase activation, immediate early gene expression, as well as NF-kappaB and AP-1 activation; it also inhibits intimal hyperplasia after balloon vascular injury in the rat, indicating the therapeutic potential for treating restenosis after arterial injury.
3. Esculetin induces apoptosis during the late stage of differentiation, it can alter fat cell number by direct effects on cell viability, adipogenesis, and apoptosis in 3T3-L1 cells.
4. Esculetin exhibits competitive inhibition against the oxidation of 3-(3,4-dihydroxyphenyl)- alanine by mushroom, the IC50 value of esculetin is 43 microM.
5. Esculetin reduces the incidence of liver lesions induced by t-BHP, including hepatocyte swelling, leukocyte infiltration, and necrosis, speculates that esculetin may play a chemopreventive role via reducing oxidative stress in living systems.
6. Esculetin suppresses proteoglycan metabolism by inhibiting the production of matrix metalloproteinases in rabbit chondrocytes, suggests that it is a therapeutically effective candidate for inhibition of cartilage destruction in osteoarthritis and rheumatoid arthritis.
1. Sinomenine has 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.
2. Sinomenine exerts anti- rheumatoid arthritis action probably through modulating the frequencies of Treg cells and Th17 cells in intestinal lymph nodes and yielding a trafficking of lymphocytes (especially Treg cells) from gut to joint.
3. Sinomenine plays the protective effects through inhibition of microglial inflammation, and the findings also provides a novel therapy to treat ICH induced brain injury.
4. Sinomenine has anti-inflammatory and neuroprotective activities through inhibition of microglial NADPH oxidase.
5. Sinomenine can prevent galactosamine (GalN)/lipopolysaccharide (LPS) -treated hepatic failure by suppressing TNF production and/or reactive oxygen generation.
1. Momordin Ic might represent a potential source of anticancer candidate, by inducing apoptosis through oxidative stress-regulated mitochondrial dysfunction involving the MAPK and PI3K-mediated iNOS and HO-1 pathways.
2. Momordin Ic and oleanolic acid obtained from KF appear to contribute to alleviating the adverse effects of CCl4 treatment by enhancing the hepatic antioxidant defense system.
3. Momordin Ic 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.
4. Momordin Ic inhibited gastric emptying , is relative to serum glucose and, at least in part, mediated by capsaicin-sensitive sensory nerves and the central nervous system.
1. Vitexicarpin can significantly reduce vascular inflammation, through inhibition of ROS-NF-κB pathway in vascular endothelial cells.
2. Vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.