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. Sinensetin is a polymethoxylated flavonoids in citrus fruit, as a novel antiangiogenesis agent, has potential for anti-carcinogenesis, antitumor, and cardiovascular protective activity.
2. Sinensetin has antioxidative effect and has anti-inflammatory by regulating the protein level of inhibitorκB-α, which may be utilized in the development of novel anti-inflammatory treatments.
3. Sinensetin enhances activation of protein kinase A and increases intracellular cAMP levels in 3T3-L1 preadipocytes, it stimulates lipolysis via a cAMP pathway in mature 3T3-L1 adipocytes, suggests that sinensetin enhances adipogenesis and lipolysis by increasing cAMP levels in adipocytes.
1. Ligustrazine Hydrochloride has certain protection effect on the vascular endothelium undergoing cardiopulmonary bypass (CPB), and lower excessive activation of coagulation reaction and inflammation reaction in patients undergoing CPB.
2. Ligustrazine hydrochloride can inhibit the activation of humai platelet following severe brain injury , improve t'ie balance, of TXA2 - PGI2 within the circulatory blood, suggests that it may be used as one of the agents to treat brain injury.
3. Ligustrazine Hydrochloride can exert down-regulate effects on Colon26 secretion of immunosuppressors and its tumor immunosuppression, one of the mechanisms is reducing tumor immunosuppression of Colon26 through decreasing its secretion of immunosuppressors.
4. Ligustrazine hydrochloride injection has antithrombotic effect on the model of induced arteriovenous shunt thrombosis.
5. Ligustrazine Hydrochloride has a protective effect on homocysteine-injured ECV304 cells.
1. Parthenolide activates both apoptosis pathway and AMPK-autophagy survival pathway through the generation of ROS, and that suppression of AMPK or autophagy can potentially enhance the anti-cancer effect of Parthenolide on breast cancer cells.
2. Parthenolide inhibits osteoclast differentiation and bone resorbing activity by down-regulation of NFATc1 induction and c-Fos stability, during RANKL-mediated osteoclastogenesis.
3. Parthenolide has in vitro activity against Leishmania amazonensis.
4. Parthenolide exhibits a variety of anti-inflammatory and immunomodulatory effects, it can attenuate LPS-induced fever, circulating cytokines and markers of brain inflammation in rats, has the potential to reduce brain inflammation.
5. Parthenolide inhibits nociception and neurogenic vasodilatation in the trigeminovascular system by targeting the TRPA1 channel, may contribute to the antimigraine effect of parthenolide.
6. Parthenolide, an inhibitor of the nuclear factor-kappaB pathway, cam ameliorate cardiovascular derangement and outcome in endotoxic shock in rodents.
1. Ophiopogonin D plays a protective role as an effective antioxidant in H2O2-induced endothelial injury, it can be therefore developed as a novel drug for the therapy of cardiovascular disorders.
2. Ophiopogonin D can attenuate doxorubicin-induced autophagic cell death by relieving mitochondrial damage in vitro and in vivo.
3. Ophiopogonin D and spicatoside A can increase mucin production and secretion, by directly acting on airway epithelial cells, they could be as expectorants in diverse inflammatory pulmonary diseases.
4. Ophiopogonin D inhibits MCF-7 cell growth via the induction of cell cycle arrest at the G2/M phase.