Anti-osteoporosis agent-4 (Compound 11h) suppresses the differentiation of primary osteoclasts and attenuates RANKL-induced osteoclastogenesis. It effectively inhibits osteoclast formation, demonstrating an IC50 value of 358.29 nM, and impedes the activation of the PI3K/AKT and IκBα/NF-κB signaling pathways [1].

Anti-inflammatory agent 50 (compound a1), a derivative of Fusidic acid, exerts its effects through inhibition of inflammatory mediators including NO, IL-6, and TNF-α. It mitigates acute lung injury by modulating these mediators and suppressing the MAPK, NF-κB, and NLRP3 inflammasome signaling pathways [1].

Caffeic Acid Phenethyl Ester (Phenylethyl Caffeate) (CAPE) inhibits the activation of nuclear transcription factor NF-kappa B and may suppress p70S6K and Akt-driven signaling pathways, with antineoplastic, cytoprotective and immunomodulating activities. CAPE is the phenethyl alcohol ester of caffeic acid and a bioactive component of honeybee hive propolis. In addition, CAPE inhibits PDGF-induced proliferation of vascular smooth muscle cells through the activation of p38 mitogen-activated protein kinase (MAPK) and hypoxia-inducible factor (HIF)-1alpha and subsequent induction of heme oxygenase-1 (HO-1).

1. Neferine ((-)-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.

Sulfuretin is a potent anti-oxidant, has protective effect against t-BHP-induced oxidative damage in human liver-derived HepG2 cells is attributable to its ability to scavenge ROS and up-regulate the activity of HO-1 through the Nrf2/ARE and JNK/ERK signa