1. Glabridin may serve as an anti-inflammatory agent in diabetes-related vascular dysfunction,through regulating the synthesis and activity of iNOS under high-glucose levels; may possess a therapeutic effect on metabolic disorders( such as diabetes and hyperglycemia), by modulating glucose metabolism through AMPK in skeletal muscle cells.
2. Glabridin may have potential as a chemopreventive agent against liver cancer metastasis, by inhibiting the invasion of human HCC cells.
3. Glabridin inhibits Plasmodium falciparum growth in vitro with an IC50 23.9±0.43 uM, it is suitable for developing antimalarial agent from a cheap and sustainable source.
4. Glabridin has not only the inhibition of melanogenesis but also the inhibition of inflammation in the skins.
5. Glabridin has antioxidative effects.
6. Glabridin and its derivatives exhibit varying degrees of estrogen receptor agonism and demonstrate growth-inhibitory actions on breast cancer cells.
7. Glabridin has a neuroprotective effect via modulation of multiple pathways associated with apoptosis.
1. Catalpalactone can inhibit dopamine biosynthesis by reducing tyrosine hydroxylase (TH) and aromatic-l-amino acid decarboxylase (AADC) activities and enhance L-DOPA- induced cytotoxiciy in PC12 cells.
2. Catalpalactone displays good cytotoxicity activities against two human tumor cell lines(MCF-7,BxPC3).
3. Catalpalactone exhibits significant inhibitory activity against 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced Epstein-Barr virus early antigen (EBV-EA) activation in Raji cells.
4. Catapalactone exhibits potent inhibitory effects on lipopolysaccharide-induced NO synthesis in RAW 264.7 cells , with IC50 values of 9.80 microM.
5. Catalpalactone exhibits high antitermitic activity.
1. Ginsenoside Rh3 is a bacterial metabolite of Rg5, has anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.
2. Ginsenosides Rh3 and Rg5 can suppress swelling of oxazolone-induced mouse ear contact dermatitis, ginsenoside Rh3 may improve chronic dermatitis or psoriasis by the regulation of IL-1β and TNF-α produced by macrophage cells and of IFN-γ produced by Th cells.
3. Ginsenoside-Rh2 and Rh3 can induce differentiation of HL-60 cells into granulocytes and modulation of PKC isoform levels may contribute to differentiation of HL-60 cells by G-Rh2.
4. Ginsenosides Rg5 and Rh3 inhibit acetylcholinesterase activity in a dose-dependent manner, with IC50 values of 18.4 and 10.2 uM, respectively, they may protect memory deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.
1. Hirsutanonol or oregonin as an active ingredient composition for treating atopic dermatitis.
2. Hirsutanonol shows significant inhibitory effects on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cyclooxygenase-2 (COX-2) expression in immortalized human breast epithelial MCF10A cells.
3. Hirsutanonol has potent antioxidant activity, it shows significant free radical scavenging activity and exhibits inhibition effect on the mitochondrial lipid peroxidation.
4. Hirsutanonol shows potent cytotoxic activities against murine B16 melanoma cells and human SNU-C1 gastric cancer cells.
5. Hirsutanonol has chemoprotective effect on human lymphocytes DNA.
6. Hirustenone and hirsutanonol show promising anti-filarial activity both in vitro and in vivo studies.
1. Fingolimod hydrochloride is an oral sphingosine-1-phosphate analogue that was approved by the FDA in 2010 for the treatment of relapsing forms of multiple sclerosis (MS)， fingolimod hydrochloride is generally well tolerated but requires diligence in patient selection and monitoring. Additional information is needed regarding risk of infection, malignancy and rebound disease with long-term use of fingolimod.
2. The gels containing 0.50% fingolimod hydrochloride (FNGL) and FNGL 0.50% plus 6% colloidal oatmeal have potential for the treatment of atopic dermatitis (AD), the presence of colloidal oatmeal may provide additional benefits.
3. Fingolimod hydrochloride can suppress inflammatory reaction of injured blood vessels and lessen the stenosis of injured blood vessels by regulating cyclooxygenase 2 and prostaglandin E2 mRNA expression using sphingosine1-phosphate receptor 1.
4. Fingolimod hydrochloride , a pak1 activator, can inhibit astemizole-induced hypertrophy and cytotoxicity in H9c2 cells, suggests that antihistamine-induced cardiac adverse effects are associated with pak1 expression and function.