kamebakaurin and Neuritis

Compelling evidence supports the notion that the majority of neurodegenerative diseases are associated with microglia-mediated neuroinflammation. Therefore, quelling of microglial activation may lead to neuronal cell survival. The present study investigated the effects of Kamebakaurin (KMBK), a kaurane diterpene isolated from Isodon japonicus HARA (Labiatae), on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated cytotoxicity in rat primary microglial cultures and the BV-2 cell line. KMBK significantly inhibited the LPS-induced production of nitric oxide (NO) in a concentration-dependent fashion in activated microglial cells. The mRNA and protein levels of inducible nitric oxide synthase (iNOS) and cyclooxycenase-2 (COX-2) were also decreased dose-dependently. Furthermore KMBK inhibited the JNK and p38 mitogen-activated protein kinases (MAPKs) in LPS-stimulated BV-2 microglial cells. Considering the results obtained, the present study authenticated the potential benefits of KMBK as a therapeutic target in ameliorating microglia-mediated neuroinflammatory diseases.

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents, Non-Steroidal; Cell Line, Transformed; Cells, Cultured; Cerebral Cortex; Diterpenes; Enzyme Activation; Isodon; JNK Mitogen-Activated Protein Kinases; Lipopolysaccharides; Mice; Microglia; Neuritis; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Protein Kinase Inhibitors; Protein Processing, Post-Translational; Rats; Rats, Sprague-Dawley; Signal Transduction; Substantia Nigra