1. 2-endo-Hydroxy-1,8-cineole shows antimicrobial and bactericidal activities against against test bacteria (Staphylococcus aureus, Escherichia coli, and Pseudomonas fluorescens) .
1. 2-Hydroxy-3-methylanthraquinone enhances apoptosis of U937 cells,in part,through activation of p-p38MAPK and downregulation of p-ERK1/2; triggers caspase-3 activation mediated apoptotic induction.
2. 2-Hydroxy-3-methylanthraquinone enhances apoptosis of THP-1 cells, in part, through activation of Fas/FasL, DR4 and TRAIL; triggers caspase-8 activation mediated apoptotic induction.
1. The recombinant protein exhibits high FNS I activity catalyzing the conversion of naringenin to apigenin and 2-Hydroxynaringenin.
1. 3,4,5-Tricaffeoylquinic acid may attenuate the TNF-α- and LPS-stimulated production of inflammatory mediators in keratinocytes by suppressing the Toll-like receptor 4 expression-mediated activation of the Akt, ERK and NF-ĸB pathways, it may exert an inhibitory effect against the pro-inflammatory mediator-induced skin disease.
2. 3,4,5-Tricaffeoylquinic acid may attenuate the proteasome inhibitor-induced programmed cell death in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways, the effect be attributed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
1. 3,4-Dihydroxybenzaldehyde has been shown to inhibit the growth of Gloeosporium musarum, a fungus which causes ripe fruit rot in the banana.
2. 3,4-Dihydroxybenzaldehyde can inhibit oxidative DNA damage and apoptosis via its antioxidant activity.
3. 3,4-Dihydroxybenzaldehyde inhibits the phosphotransferase activity of CKII with IC(50) of about 783 microM, it may function by inhibiting oncogenic disease, at least in part, through the inhibition of CKII activity.
4. 3,4-Dihydroxybenzaldehyde inhibits the H2O2-induced apoptosis of granulosa cells, promotes estradiol secretion in granulosa cells and enhanced the mRNA expression levels of steroidogenic factor 1, a promoter of key steroidogenic enzymes.
5. 3,4-Dihydroxybenzaldehyde has tyronase inhibitory effect.
1. 3,4-Dihydroxybenzoic acid exhibits scavenging actions against the 1,1-diphenyl-2-picrylhydrazyl radical, the superoxide anion, and the hydroxyl radical.
2. 3,4-Dihydroxybenzoic acid isolates from a green alga protects human keratinocytes against UVB-induced oxidative stress and apoptosis.
3. The 3,4-Dihydroxybenzoic acid treatment resulted in 33.3, 65.0, 76.7 and 85.0% hatch inhibition at 0.125, 0.25, 0.5 and 1.0 mg/ml, respectively, 3 days after incubation.
1. 3,6'-Disinapoyl sucrose has neuroprotective effect and antidepressive activity in rats, at least in part, by increasing expression of cyclic AMP response element (CRE)-binding protein (CREB) and its downstream target protein, brain-derived neurotrophic factor (BDNF).
2. Treatment with 3,6'-Disinapoyl sucrose (0.6, 6, and 60 μmol/L) increases cell viability dose dependently, inhibits LDH release, and attenuated apoptosis. The mechanisms by which 3,6'-Disinapoyl sucrose protect neuron cells from glutamate-induced excitotoxicity include the downregulation of proapoptotic gene Bax and the upregulation of antiapoptotic gene Bcl-2.
1. (Z)-3-butylidenephthalide has antihyperglycemic effect is due to inhibition of α-glucosidase at the intestinal level, inhibited the activity of yeast-α-glucosidase (IC(50) 2.35 mM) in a noncompetitive fashion with a K(i) of 4.86 mM.
2. Z-3-Butylidenephthalide can induce a dose-dependent antinociceptive action in the hot-plate assay, it is also effective for controlling the pain provoked by chemical irritation at the doses of 10 and 31.6 mg/kg.
1. 3-Deoxysappanchalcone is an effective HO-1 inducer at the translational level.
2. 3-Deoxysappanchalcone has anti-inflammatory effects, is a valuable compound for modulating inflammatory conditions.
3. 3-Deoxysappanchalcone has anti-influenza virus activity, the mechanism involved anti-apoptosis and anti-inflammation activities in vitro.
4. 3-Deoxysappanchalcone has inhibitory activity on MMP-9 expression and production in TNF-α-treated cells, is mediated by the suppression of AP-1 and NF-κB activation.