1. 20(R)-Ginsenoside Rh2, a minor stereoisomer of ginsenoside Rh2, possesses matrix metalloproteinase inhibitory.
2. 20(R)-Ginsenoside Rh2 has a significant inhibitory effect on the proliferation.
3. 20(R)-Ginsenoside Rh2 has anti-inflammatory and antioxidative activities.
4. 20(R)-Ginsenoside Rh2 shows selective osteoclastgenesis inhibitory activity without any cytotoxicity up to 100 microM.
5. 20 (R)-ginsenoside Rh2 and 20(S)-ginsenoside Rh2 have anticancer effects and can increase inchoate apoptotic rate, reduce apoptotic rate significantly, enhance the activity of caspase-3 and induces apoptosis in human lung adenocarcinoma A549 cells.
1. Ginsenoside Rh2 (G-Rh2) can inhibit cancer proliferation, protect differentiation in certain cancer cells.
2. G-Rh2 inhibits the growth of A375-S2 cells in vitro by inducing apoptosis partially dependent on caspase-8 and caspase-3 pathway.
3. G-Rh2 exhibits antiallergic activity originating from cell membrane-stabilizing activity and antiinflammatory activity by the inhibition of NO and PGE2 production.
1. 20-Hydroxyecdysone has immunomodulatory, hepatoprotective, anti-arrythmic, and cholesterol-lowering properties.
2. 20-Hydroxyecdysone as ingredients in nutritional supplements for various sports, particularly bodybuilding.
3. 20-Hydroxyecdysone induces autophagy and caspase activity, predominantly transduced by E93 in the remodeling fat body of Drosophila.
4. 20-Hydroxyecdysone (via GPCR activation and calcium signaling) activates CaMKII phosphorylation and nuclear translocation, which regulate USP1 lysine acetylation to form an EcRB1-USP1 complex for 20E response gene transcription.
1. Ginsenoside Rg2 can protect H9c2 cells against H2O2- induced injury through its actions of anti-oxidant and anti-apoptosis.
2. Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3βand induction of SHP gene expression, it may have a therapeutic potential for type 2 diabetic patients.
3. 20R-Ginsenoside Rg2 inhibits the cytokine interleukin 1 alpha (IL-1α)-induced reduction in gap junction-mediated intercellular communication (GJIC).
1. 24-Methylenecycloartan-3-o l has inhibitory effects on HIV-1 protease.
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 can scavenge DPPH radical, hydroxyl radical and intracellular ROS.
2. 3,4-dihydroxybenzaldehyde chelated Fe2+.
3. 3,4-dihydroxybenzaldehyde attenuated H2O2-induced cell death and apoptosis.
4. 3,4-dihydroxybenzaldehyde inhibits oxidative DNA damage and its treatment decreased the expression level of phospho-H2A.X.
5. Electrocatalysis of NADH Oxidation with Electropolymerized Films of 3,4-Dihydroxybenzaldehyde.
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.