1. Polydatin is a mitochondria protector for acute severe hemorrhagic shock treatment, the neuronal mitochondrial injury is involved in the genesis of severe shock and polydatin may be the best choice for protection of neuron against mitochondrial injury in severe shock.
2. Polydatin has favorable potency to develop a hypolipemic and/or hepatoprotective agent in clinic.
3. Polydatin has a protective effect against ischemia/reperfusion injury in rat heart, the cardioprotection of polydatin is mainly mediated by cNOS which leading to an increase in NO production.
4. Polydatin is a natural precursor of resveratrol, it can induce β-defensin production and reduce inflammatory response, they reinforce cytoprotective response in stress conditions and suggest their use in cosmetic or pharmaceutical preparations.
5. Polydatin modulates inflammation by decreasing NF-κB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.
6. Polydatin has antioxidant activity.
7. Polydatin inhibits growth of lung cancer cells by inducing apoptosis and causing cell cycle arrest.
1. Coptisine chloride can be absorbed across intestinal epithelial cells, and completely absorbed compounds.
2. Coptisine exerts pronounced cardioprotection in rats subjected to myocardial I/R likely through suppressing myocardial apoptosis and inflammation by inhibiting the Rho/ROCK pathway, suggests that it protects rat heart against myocardial ischemia/reperfusion injury by suppressing myocardial apoptosis and inflammation.
1. Schisantherin A exhibits anti-inflammatory and antioxidant effects, it can significantly attenuate Aβ1-42-induced learning and memory impairment and noticeably improve the histopathological changes in the hippocampus, it could serve as a potential agent in treatment of Alzheimer's disease.
2. Schisantherin A can protect against myocardial ischemia-reperfusion injury, the underlining mechanism may be related to its role in inhibiting cardiomyocyte apoptosis.
3. Schisantherin A shows anti-inflammatory potentials, it may inhibit LPS-induced production of inflammatory cytokines by blocking NF-kappaB and MAPKs signaling in RAW264.7 cells.
4. 100 muM of Deoxyschizandrin and schisantherin A exhibit strong inhibition on UDP-glucuronosyltransferases (UGTs)1A3, suggests that herb-drug interaction may occur when deoxyschizandrin or schisantherin A containing herbs were co-administered with drugs which mainly undergo UGT1A3-mediated metabolism.
5. Schisantherin A has been used as an antitussive, tonic, and sedative agent, it also can attenuate osteoclast formation and wear particle-induced osteolysis by mediating RANKL signaling pathways, indicates that it is a promising therapeutic natural compound for the treatment of osteoclast-related prosthesis loosening.
6. Schisantherin A exhibits neuroprotection against 1-methyl-4-phenylpyridinium ion (MPP(+)) through the regulation of two distinct pathways including increasing CREB-mediated Bcl-2 expression and activating PI3K/Akt survival signaling, suggests that it may be a promising neuroprotective agent for the prevention of Parkinson's disease.
1. Ginsenoside Rb3 has protective effects on oxygen and glucose deprivation-induced ischemic injury in PC12 cells.
2. Ginsenoside Rb3 possesses the effect against isoproterenol-induced myocardial injury and heart function impairment, and that the mechanism is related to its antioxidant activity at least in part.
3. Ginsenoside Rb3 shows protective effect on the OGD-Rep injury is attributed to the inhibition of JNK-mediated NF-κB activation, suggests that it has the potential to serve as a novel therapeutic agent for myocardial I/R injury.
4. Ginsenoside Rb3 may have antidepressant-like effects, brain-derived neurotrophic factor and the monoamine neurotransmitters 5-hydroxytryptamine, dopamine, and norepinephrine are involved in ginsenoside Rb3's antidepressant-like effects.
5. Ginsenoside Rb3 significantly attenuates the changes of creatine kinase activity and lactate dehydrogenase activity.
6. Ginsenoside Rb3 can exert a neuroprotective role on hippocampal neurons, a role which was partly mediated by the facilitation of Ca2+-dependent deactivation of NMDA receptors, and the resultant reduction of intracellular free Ca2+ level.
7. Ginsenoside Rb3 reduces fasting blood glucose level, food intake, water intake, improved oral glucose tolerance, and repaired injured pancreas tissues of alloxan-induced diabetic mice, suggests that ginsenoside possesses the potential of the clinical use in preventing and treating diabetes.
1. Protopanaxdiol is effective in preventing and healing obesity, fatty liver and hypertriglyceridemia in mice fed with a high-fat diet.
2. Protopanaxdiol has the effect of anti-tumor through increasing the activity of body immunity,improving the lymphocyte transformation,the activity of NK cells and the contents of IL-2 significantly.
3. Protopanaxdiol inhibits tumor interstitial microvascular density and its proliferation activity, finally inhibits tumor growth.
4. Protopanaxdiol can inhibit expression of vascular endothelial growth factor (VEGF) and basofibroblast growth factor(bFGF) protein,finally inhibits tumor growth of liver.
5. (20R)-Protopanaxdiol has protective effect on myocardial ischemia, which may be related to improving free radicals metabolism and myocardial metabolism, decreasing plasma TXA 2 levels.