1. Astragaloside IV has antioxidant and anti-aging activities.
2. Astragaloside IV protects dopaminergic neurons.
3. Astragaloside IV has anti-fibrotic effect against systemic sclerosis.
4. Astragaloside IV has anti-inflammatory activity, the mechanism may be inhibiting the NF-kappaB pathway.
5. Astragaloside IV inhibits migration and invasion in human lung cancer A549 cells via regulating PKC-α-ERK1/2-NF-κB pathway.
1. Sophocarpine is an effective agent for treating colonic inflammation.
2. Sophocarpine is a human ether-à-go-go-related gene (HERG) inhibitor with an IC(50) of about 0.2 mM.
3. Sophocarpine has anti-inflammatory effect, reduces synthesis of inflammatory cytokines TNF-α, TGF-β1 and IL-6 and inhibits translocation of NF-κB.
4. Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway, may be a potential chemotherapeutic agent for chronic liver diseases.
5. Sophocarpine could decrease the level of serum transaminase, improve lipid metabolism, activate protective adipocytokine adiponectin, may be as a promising agent for the clinical prevention and therapy of NASH.
1. Conophylline is useful in inducing differentiation of pancreatic β cells both in vivo and in vitro.
2. Conophylline down-regulates the expression of the TNF-alpha receptors on the cell surface, inhibits TNF-alpha-induced NF-kappaB activation.
3. Conophylline shows potential for treatment of type 1 diabetes, as well as a possible therapeutic role in pancreatic cancer.
4. Conophylline increased the expression of mRNA for insulin and the number of pancreatic duodenal homeobox-1-positive cells. These effects of conophylline were similar to those of activin A.
1. Neotuberostemonine ia has antitussive activity.
1. Neferine has anti-tumor activities , Metabolic activation mediated by CYP3A4 and GSH depletion enhanced Neferine-induced cytotoxicity.
2. Neferine can be helpful to increase the efficacy of DOX and to achieve anticancer synergism by curbing the toxicity.
3. Neferine inhibited high glucose-induced endothelial apoptosis via blocking ROS/Akt/NF-κB pathway, which provides the evidence for using Neferine to treat diabetic vasculopathy.
4. Neferine induced apoptosis in a dose-dependent manner with the hypergeneration of reactive oxygen species, activation of MAPKs, lipid peroxidation, depletion of cellular antioxidant pool, loss of mitochondrial membrane potential, and intracellular calcium accumulation.