1. Alpha-hederin is a haemolytic agent.
2. Alpha-hederin has potential anti-inflammatory activity.
3. Alpha-hederin shows molluscicidal activity and antifungal activity.
1. Alpha-mangostin has antioxidant and anti-inflammatory activities.
2. Alpha-mangostin has strong antifungal activity and low toxicity to make it a promising agent for treatment of oral candidiasis.
3. Alpha-mangostin exhibits peripheral and central antinociception through modulation of opioid and vanilloid receptors, the glutamatergic system, and the larginine/NO/cGMP/PKC/K(+)-ATP pathways.
4. Alpha-mangostin has anti-cancer activity, can reduce cell proliferation and inhibit tumorigenesis, by inducing apoptosis via the mitochondrial pathway1, blockade of Stat3 signaling pathway, and inhibiting Fatty acid synthase (FAS).
1. Alpha-Solanine alters antioxidative enzyme activities and MDA and PCO concentrations and GST activity in fat body and midgut.
2. Alpha-Solanine has proliferation-inhibiting and apoptosis-promoting effect on multiple cancer cells, such as clone, liver, melanoma cancer cells.
1. Alpha-Spinasterol is characterized by good blood-brain permeability.
2. Alpha-Spinasterol is a novel efficacious and safe antagonist of the TRPV1 receptor with antinociceptive effect.
3. Alpha-Spinasterol can prevent TP-induced prostatic hyperplasia and may be beneficial in the management of benign prostatic hyperplasia.
1. Alpha-Tocopherolquinone has a favorable pharmacokinetic profile when administered orally with food.
2. Alpha-Tocopherolquinone cannot replace endogenous ubiquinones in the respiratory chain function, nevertheless it can be reduced by the mitochondrial respiratory chain substrates, presumably through the reduced ubiquinones.
3. Alpha-Tocopherolquinone has antioxidant effect, can inhibit lipid peroxidation and reduce cell division in both the glioma cell clone and fetal brain cells.
1. Alpha-Viniferin inhibits AChE activity is specific, reversible and noncompetitive, in a dose-dependent manner, and the IC50 values of alpha-Viniferin were 2.0 microM.
2. Alpha-Viniferin exhibits a dose-dependent inhibition on cyclooxygenase activity, where 50% of inhibition (IC50) was shown at a final concentration of about 7 microM.
3. Alpha-Viniferin has anti-inflammatory activity, down-regulating STAT-1-inducible inflammatory genes via inhibiting ERK-mediated STAT-1 activation in IFN-gamma-stimulated macrophages.
1. Alpinetin has antibacterial activity.
2. Alpinetin has anti-inflammatory activity.
3. Alpinetin can enhance the sensitivity of HepG2 hepatoma cells to the chemotherapeutic agent CDDP.
4. Alpinetin has strong anti-hepatoma and pancreatic cancer cells effects, by inhibiting proliferation ,regulating of the Bcl-2 family and XIAP expression, releasing of cytochrome c and activating caspases.
1. Alpinumisoflavone has atheroprotective effects, may result from their ability to upregulate mechanisms promoting HDL-cholesterol and bile acid formation.
2. Alpinumisoflavone is endowed with estrogenic properties accounting, at least in part, for E. lysistemon effects.
3. Alpinumisoflavone induces cell death, may be via repressing both the ERK/MAPK and NF-κB pathways.
1. Alstonine is an indole alkaloid that has an antipsychotic activity, by decreasing glutamate uptake and using the step-down inhibitory avoidance paradigm and MK801-induced working memory deficits in mice.
2. Alstonine prevents the expected fasting-induced decrease in glucose levels.
1. Amentoflavone can interact with many other medications by being a potent inhibitor of CYP3A4 and CYP2C9, which are proteins used for drug metabolism in the body, is an inhibitor of human cathepsin B.
2. Amentoflavone has antimalarial activity in trials significant affinities towards the delta-1, kappa opioid receptors (as an antagonist) and binds to benzodiazepine receptors.
3. Amentoflavone may be a potential lead for a new type of anti-inflammatory agents having dual inhibitory activity of group II phospholipase A2 and cyclooxygenase.
4. Amentoflavone and quercetin differentially exerted supression of PGE2 biosynthesis via downregulation of COX-2/iNOS expression.