1. 6,7,4'-Trihydroxyisoflavone has antioxidant activity.
2. 6,7,4'-Trihydroxyisoflavone, is a novel inhibitor of PKCα in suppressing solar UV-induced matrix metalloproteinase 1.
3. 6,7,4'-trihydroxyisoflavone, suppresses adipogenesis in 3T3-L1 preadipocytes via ATP-competitive inhibition of PI3K.
4. 6,7,4'-trihydroxyisoflavone inhibits HCT-116 human colon cancer cell proliferation by targeting CDK1 and CDK2.
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. 6,8-Diprenylgenistein has antimicrobial activity .
2. 6,8-Diprenylgenistein has anti-bacteria activity against Gram-negative and Gram-positive bacteria.
1. 6,8-Diprenylorobol possesses weaker anti-H. pylori activity, may be used as chemopreventive agent for peptic ulcer or gastric cancer.
2. 6,8-Diprenylorobol is evaluated against the AIDS-related opportunistic fungal pathogens, Candida albicans and Cryptococcus neoformans.
1. 6-Gingerol has been known to possess anti-tumorigenic and pro-apoptotic activities, it stimulates apoptosis through upregulation of NAG-1 and G1 cell cycle arrest through downregulation of cyclin D1, multiple mechanisms appear to be involved in 6-gingerol action, including protein degradation as well as β-catenin, PKCε, and GSK-3β pathways.
2. 6-Gingerol and 6-shogaol may both exert anti-invasive activity against hepatoma cells through regulation of MMP-9 and TIMP-1, inhibition of the MAPK and PI3k/Akt pathways and NF-κB and STAT3 activities to suppress expression of MMP-2/-9 and uPA and block angiogenesis, and that 6-shogaol could further regulate urokinase-type plasminogen activity.
3. 6-Gingerol can repress quorum sensing (QS)-induced genes, specifically those related to the production of virulence factors, inducing exoprotease, rhamnolipid, and pyocyanin.
4. 6-Gingerol has antioxidant and anti-inflammatory activities, it induces genotoxicity probably by oxidative stress; lysosomal and mitochondrial damage were observed in 6-gingerol-induced toxicity.
5. 6-Gingerol has anti-adipogenic activity , can effectively suppress adipogenesis and that it exerts its role mainly through the significant down-regulation of PPARγ and C/EBPα and subsequently inhibits FAS and aP2 expression, also inhibit differentiation in 3T3-L1 cells by attenuating the Akt/GSK3β pathway.
1. 6-Hydroxykaempferol is a competitive inhibitor of tyrosinase compared to L-DOPA, it shows also high antioxidant activities.
1. 6-Hydroxykaempferol 3,6-di-O-glucoside and 6-hydroxykaempferol 3,6,7-tri-O-glucoside can inhibit platelet aggregation induced by collagen, they also show weak inhibitory effects on the adenosine 5'-diphosphate (ADP)- induced platelet aggregation.