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. 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.
1. Ampelopsin inhibits EMT and reduces the invasion of ovarian cancer cells via the NF-κB/Snail pathway.
2. Ampelopsin is an effective mTOR inhibitor ,can induce protective autophagy in human breast cancer cells through Akt-mTOR pathway via ER stress.
3. Ampelopsin exerts anti-arrhythmic effects in this rat model, and the underlying electrophysiological mechanism is partly associated with the inhibition of INa and enhancement of IK1, and prolongation of APD.
1. Amygdalin has antitumor activity against cervical cancer, by inhibiting the growth of HeLa cell xenografts through a mechanism of apoptosis.
2. Amygdalin is a potent antifibrotic agent that may have therapeutic potential for patients with fibrotic kidney diseases.
3. Amygdalin joint HSYA could inhibit the degeneration of the endplate chondrocytes derived from intervertebral discs of rats induced by IL-1beta and better than the single use of Amygdalin or HSYA.
1. Anemarsaponin B can inhibit PAF-induced rabbitplatelet aggregation in vitro.
1. Anethole has antispasmodic, cardiovascular,and gastroprotective effects.
2. Anethole blocks neuronal excitability,and induces the blockade of neuromuscular transmission .
3. Anethole can act as the CXCR4 antagonist and as the PTEN activator which resulted to PI3K/AKT-mediated inhibition of the metastatic prostate cancer progressions.
4. Anethole prevents LPS-induced acute lung inflammation in mice, may be therapeutically effective in inflammatory conditions in humans.
5. Anethole may have a potent inhibitory effect on PD through suppression of pro-inflammatory molecules, it could be a novel therapeutic strategy for Periodontitis.
6. Anethole-induced cell death could be explained by oxidative stress-dependent apoptosis via typical mitochondrial death cascades in fungi, including A. fumigatus and S. cerevisiae.
1. Angelicin may provide a lead structure for the development of antiviral drug against gammaherpesviruses.
2. Angelicin might be a potential new agent for prevention of inflammatory reactions and diseases in the clinic.
3. Angelicin is an effective apoptosis-inducing natural compound of human SH-SY5Y neuroblastoma cells.
4. Angelicin, at high seed productivity of H. sosnowskyi may have an ecological significance in plant-plant interaction.
1. Angustifoline has activity against gram-positive bacteria.
1. Annonacin is mitochondrial complex I inhibitor, reported to be more toxic than rotenone to mesencephalic neurons; can cause significant cell death in various cancer cell lines..
2. Annonacin induces growth arrest and apoptosis in ERα-related pathways in MCF-7 cells, attenuates MCF-7 xenograft tumor growth while inhibiting ERα, cyclin D1 and Bcl-2 protein expressions in nude mice.
3. Annonacin-induced ATP depletion causes the retrograde transport of mitochondria to the cell soma and induces changes in the intracellular distribution of tau in a way that shares characteristics with some neurodegenerative diseases.