Turmerones are a component of turmeric essential oil, and have many of the same properties as curcumin. While they are well known to enhance the absorption of curcumin, they also have strong anti-inflammatory, anti-oxidant, and potential anti-tumor abilities of their own.
Researchers are especially interested in aromatic turmerone, most often referred to as “ar-turmerone.” In good news for anyone who has cognitive health concerns—a history of Alzheimer’s or dementia in their family background, for instance—ar-turmone may offer hope.
Amyloid beta plaques in the brain that block neural signals are implicated as being one of the causes of Alzheimer Disease and other degenerative cognitive conditions. One of the causes behind the formation of these plaques is inflammation, which is further spurred along by the amyloid beta cells themselves. Ar-turmerone suppressed inflammatory cytokines and oxidative stress in brain cells. While more research is required, it shows that this compound from turmeric may become a new, powerful botanical intervention to treat individuals with cognitive disorders.
Park SY, Jin ML, Kim YH, Kim Y, Lee SJ. Anti-inflammatory effects of aromatic-turmerone through blocking of NF-κB, JNK, and p38 MAPK signaling pathways in amyloid β-stimulated microglia. Int Immunopharmacol. 2012 Sep;14(1):13-20. doi: 10.1016/j.intimp.2012.06.003. Epub 2012 Jun 20.
Amyloid β (Aβ) induces the production of neuroinflammatory molecules, which may contribute to the pathogenesis of numerous neurodegenerative diseases. Therefore, suppression of neuroinflammatory molecules could be developed as a therapeutic method. Aromatic (ar)-turmerone, turmeric oil isolated from Curcuma longa, has long been used in Southeast Asia as both a remedy and a food. In this study, we investigated the anti-inflammatory effects of ar-turmerone in BV2 microglial cells. Aβ-stimulated microglial cells were tested for the expression and activation of MMP-9, iNOS, and COX-2, the production of proinflammatory cytokines, chemokines, and ROS, as well as the underlying signaling pathways. Ar-turmerone significantly suppressed Aβ-induced expression and activation of MMP-9, iNOS, and COX-2, but not MMP-2. Ar-turmerone also reduced TNF-α, IL-1β, IL-6, and MCP-1 production in Aβ-stimulated microglial cells. Further, ar-turmerone markedly inhibited the production of ROS. Impaired translocation and activation of NF-κB were observed in Aβ-stimulated microglial cells exposed to ar-turmerone. Furthermore, ar-turmerone inhibited the phosphorylation and degradation of IκB-α as well as the phosphorylation of JNK and p38 MAPK. These results suggest that ar-turmerone impaired the Aβ-induced inflammatory response of microglial cells by inhibiting the NF-κB, JNK, and p38 MAPK signaling pathways. Lastly, ar-turmerone protected hippocampal HT-22 cells from indirect neuronal toxicity induced by activated microglial cells. These novel findings provide new insights into the development of ar-turmerone as a therapeutic agent for the treatment of neurodegenerative disorders.
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