Coumestrol is a novel inducer of mitochondrial biogenesis through the activation of Sirt1, it suppresses the accumulation of HIF-1α via suppression of SPHK1 pathway in hypoxic PC-3 cells. Coumestrol can function by inhibiting oncogenic disease, at least in part, through CKII inhibition-mediated cellular senescence. Coumestrol treatment is effective in preventing neuronal loss in all times of administration as well as able to rescue the Na+, K+ -ATPase activity, suggesting its potential benefits for either prevention or therapeutics use against cerebral ischemia in males.
Alliin has antiglycating potential , it offers protection against glucose or methyglyoxal induced glycation of superoxide dismutase, hence is expected to have therapeutic potential in the prevention of glycation-mediated diabetic complications. Alliin has anti-inflammatory activity, it protects against Lipopolysaccharides (LPS)-induced acute lung injury (ALI) by activating PPARγ, which subsequently inhibits LPS-induced NF-κB activation and inflammatory response; alliin has an inhibitory effect in osteoclasteogenesis with a dose-dependent manner via blocking the c-Fos-NFATc1 signaling pathway, it could be a potential therapeutic agent in the treatment of osteoporosis. Alliin and sabinene have detectable levels of antimicrobial activity.
Kinsenoside shows significant antihepatotoxic, and anti-inflammatory activities. Kinsenoside could be useful for repairing beta cells in pancreatic islet injury as well as improving its function, it could promote the glucose tolerance of acute glucose increase in both diabetic and normal healthy rats. Kinsenoside inhibits osteoclastogenesis from macrophages by attenuating RANKL-induced NF-κB and NFATc1 activities, which in turn, prevents bone loss from OVX mice.
1-Hydroxy-2,3,4,7-tetramethoxy-xanthone has vasodilatory action, it can cause vasodilation in the coronary artery pre-contracted with 1uM 5-hydroxytryptamine (5-HT), with the EC 50 value of 6.6±1.4 uM. 1-Hydroxy-2,3,4,7-tetramethoxyxanthone can effectively inhibit the osteoclast differentiation in a co-culture system with mouse osteoblastic calvarial cells and bone marrow cells.
1-Hydroxy-2,3,5-trimethoxyxanthone (HM-1) has vasodilator action ,which involves both an endothelium-dependent mechanism involving NO and an endothelium-independent mechanism by inhibiting Ca(2+) influx through L-type voltage-operated Ca(2+) channels; a minor contribution to the effects of HM-1 may be related to inhibition of the protein kinase C-mediated release of intracellular Ca(2+) stores. HM-1,at the concentration of 1 ug/mL, can effectively inhibit the osteoclast differentiation in a co-culture system with mouse osteoblastic calvarial cells and bone marrow cells; it also can protect mice from the acute lung injury induced by ipopolysaccharide (LPS), which is relative to the increasing of IκB-α protein expression and the suppressing of inducible nitric oxide synthase and cyclooxygenase-Ⅱ protein expression.