ABSTRACT
A new iridoid glycoside, named camptoside (1), together with three known compounds as dehydrodiconiferyl alcohol-9'-O-ß-d-glucopyranoside (2), aesculetin (3) and vajicoside (4), have been isolated from Camptosorus sibiricus Rupr. (Aspleniaceae). Their structures were established on the basis of spectroscopic analysis, especially 1D- and 2D-NMR data, and by comparison of their spectroscopic and physical data with those reported in the literature. Compounds 1-3 exhibited inhibitions of nitric oxide production in lipopolysaccharide-induced RAW 264.7 macrophages with IC50 values of 11.2, 8.3 and 9.4⯵M, respectively.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Glycosides/pharmacology , Iridoids/pharmacology , Macrophages/drug effects , Tracheophyta/chemistry , Animals , Anti-Inflammatory Agents/isolation & purification , Chilaiditi Syndrome , Glycosides/isolation & purification , Iridoids/isolation & purification , Mice , Molecular Structure , Nitric Oxide/metabolism , Phytochemicals/isolation & purification , Phytochemicals/pharmacology , RAW 264.7 CellsABSTRACT
Cerebral ischemia and following reperfusion affects many people worldwide. To discover efficient therapeutic approaches, numerous natural products have been investigated. The current study investigated the protective effects of thevetiaflavone, a natural flavonoid obtained from Wikstroemia indica, and the associated mechanisms using PC12 cells induced by oxygen and glucose deprivation. As a result, thevetiaflavone improves cell viability and suppresses the leakage of lactate dehydrogenase from the cytoplasm. Further investigation of the mechanisms demonstrated that thevetiaflavone decreases overproduction of ROS and ameliorates ROSmediated mitochondrial dysfunction, including collapse of mitochondrial membrane potential and mitochondrial permeability transition pore opening. Thevetiaflavone reduces the intracellular Ca2+ level, which is closely associated with mitochondrial function and interplays with ROS. Furthermore, thevetiaflavone inhibits apoptosis in PC12 cells through upregulating the expression of Bcl2 and downregulating that of Bax and caspase3 in addition to increasing the activity of caspase3. These results further indicate the protective effects of thevetiaflavone in vivo and its application in the clinic.
