1. Koumine can induce apoptosis of LoVo cells in a time-dependent manner and inhibit the DNA synthesis in LoVo cells, thereby blocking the cell cycle from G1 to S phase.
2. Koumine has a significant analgesic effect in rodent behavioral models of inflammatory and neuropathic pain, and that the reduction in neuropathic pain may be associated with the upregulation of allopregnanolone in the spinal cord.
3. Koumine has therapeutic effect against psoriasis, which is related to the inhibition of epidermal cell proliferation, promoting the formation of granular cells and decreasing the serum level of IL-2.
4. Koumine can significantly reduce the damage to axon and myelin sheath of the sciatic nerve and increase sensory nerve conduction velocity , without affecting body weight and blood glucose, these findings encourage the use of koumine in the treatment of diabetic neuropathy.
5. Koumine has antineoplastic effect, may be a future breast cancer chemotherapeutic agent.
6. Koumine may produce anxiolytic-effect by increasing the levels of pregnenolone and allopregnenolone in hippocampus.
1. Cannabidiol can reduce the anxiety provoked by Delta-9-tetrahydrocannabinol (delta-9-THC) in normal volunteers, and the effects of cannabidiol , as opposed to those of delta 9-THC, may be involved in the antagonism of effects between the two cannabinoids.
2. Cannabidiol has a potent anti-arthritic effect in collagen-induced arthritis through its combined immunosuppressive and anti-inflammatory actions.
3. Cannabidiol has a pharmacological profile similar to that of atypical antipsychotic drugs.
4. Cannabidiol is a potent inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 microM), with significantly lower potency in noncancer cells.
5. Cannabidiol exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against beta-amyloid peptide toxicity, and that inhibition of caspase 3 appearance from its inactive precursor, pro-caspase 3, by cannabidiol is involved in the signalling pathway for this neuroprotection.
6. Cannabidiol may have great therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular disorders, by attenuating oxidative/ nitrative stress, inflammation, cell death and fibrosis.
1. (+)-Taxifolin is an inhibitor of aggregation of the 42-residue amyloid β-protein, it has preventive effects against Alzheimer's disease-like pathogenesis in vivo.
2. (+)-Taxifolin is a weak inhibitor of cytochrome b5 reduction (IC50=9.8μM).
1. Hispidulin has anti-oxidative, anti-inflammatory and anti-cancer activities, it can alleviate methamphetamine-induced hyperlocomotion without motor impairment in mice, suggesting a therapeutic potential of Hispidulin in hyper-dopaminergic disorders.
2. Hispidulin exerts anti-osteoporotic and bone resorption attenuating effects via activating the AMPK signaling pathway.
3. Hispidulin sensitizes the tumor cells to Gemcitabine and 5-Fluoroucil by down-regulating HIF-1α/P-gp signaling, it appears to be a promising and novel chemosensitizer for gallbladder cancer treatment.
4. Hispidulin has considerable antiepileptic, neuroprotective, and antiinflammatory effects on kainic acid-induced seizures in rats.
5. Hispidulin can ameliorate high glucose-mediated endothelial dysfunction via inhibiting PKCβII-associated NLRP3 inflammasome activation and NF-κB signaling, it has potential application in the prevention and treatment of diabetic vascular complications.
6. Hispidulin targets the VEGF receptor 2-mediated PI3K/Akt/mTOR signaling pathway in endothelial cells, leading to the suppression of pancreatic tumor growth and angiogenesis.
7. Hispidulin can inhibit platelet aggregation by elevating cAMP levels by a mechanism different from that of theophylline or PGE1.
1. Licarin B can improve insulin sensitivity via PPARγ and activation of GLUT4 in the IRS-1/PI3K/AKT pathway in 3T3-L1 adipocytes, it as a promising bioactive for insulin resistance and associated complications through its partial PPARγ activity.