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. Ginsenoside-Ro has anti-inflammatory activity, it (10, 50, and 200 mg/kg, p.o.) inhibits an increase in vascular permeability in mice induced by acetic acid and reduces an acute paw edema in rats induced by compound 48/80 or carrageenin.
2. Ginsenoside Ro inhibits the increase of connective tissue in the liver of CCl4-induced chronic hepatitic rats, it shows a stronger inhibitory effect on the GalN-induced acute hepatitic model than those of the aglycone of ginsenoside Ro, oleanolic acid, or glycyrrhizic acid and its aglycone, glycyrrhetinic acid.
3. Ginsenoside Ro enhances in vivo hair re-growth based on their inhibitory activity against 5αR in the androgenetic alopecia model.
4. Ginsenoside-Ro shows immunomodulatory effects by regulating the production and expression of Th1/Th2 cytokines in murine splenocytes.
5. Ginsenoside Ro exerts anti-apoptosis and anti-inflammation in IL-1β-induced rat chondrocytes, which might be related to NF-κB signal pathway, it might be a potential novel drug for the treatment of osteoarthritis.
6. Ginsenoside Ro has antioxidative properties against UV-B-induced oxidative stress in human dermal fibroblasts, it possesses a potential skin anti-photoaging property against UV-B radiation in fibroblasts.
1. Chondroitin is in dietary supplements used as an alternative medicine to treat osteoarthritis.
2. Chondroitin inhibits dose-dependently of the hydrolysis and transglycosylation reactions of bovine testicular hyaluronidase.
3. Chondroitin sulfate is a regulator of neuronal patterning in the retina, in the developing mammalian retina, gradual regression of chondroitin sulfate may help control the onset of ganglion cell differentiation and initial direction of their axons.
4. Chondroitin sulfate has anti-inflammatory and chondroprotective actions.
1. Glucosamine sulfate can stimulate proteoglycan synthesis by chondrocytes and has mild anti-inflammatory properties, it is therefore as effective as ibuprofen on symptoms of knee osteoarthritis (OA), suggests that glucosamine sulfate as a safe symptomatic Slow Acting Drug for OA.
2. Glucosamine sulfate has environmental antibacterial activity.
1. Bavachin, a phytoestrogen, potentially protects cartilage from inflammation-mediated damage in joints of osteoarthritis patients through decreasing IL-1β-induced activation of IKK-IκBα-NF-κB signaling pathway.
2. Bavachin has inhibitory effects on melanin production in B16 mouse melanoma cells, it may have suppressive effects against pigmentation by melanin in the skin.
3. Bavachin and isobavachalcone are cholesterol acyltransferase inhibitors.
4. Bavachin increases insulin-induced glucose uptake by differentiated adipocytes and myoblasts, it enhances glucose uptake via glucose transporter 4 (GLUT4) translocation by activating the Akt and 5′AMP-activated protein kinase (AMPK) pathway in the presence or absence of insulin; suggests that bavachin might have therapeutic potential for type 2 diabetes by activating insulin signaling pathways.
5. Bavachin in the blood can stimulate the genetic expression of VEGF in PB,and directly help the fracture healing, it has no significant influence on the 5-HT concentration during the fracture healing.