While turmeric is well known as a culinary ingredient and source of curcumin, it also provides turmeric essential oil, which helps curcumin absorb more efficiently and provides compounds called “turmerones” that have powerful anti-inflammatory and antioxidant abilities.
One of the most researched of these compounds is called aromatic turmerone, generally abbreviated to “ar-turmerone.” Ar-turmerone has been shown to have many applications, but an intriguing one is that it may help prevent cognitive decline by reducing the accumulation of amyloid beta plaques that can block signals in the brain. This study found that ar-turmerone inhibited a number of inflammatory markers and protected hippocampal cells (from a region in the brain associated with memory) as well.
While more research needs to be done to verify the effects in humans, this study represents real hope that the causes of cognitive decline can be slowed down, or possibly even prevented altogether. It also shows us that there is much more to turmeric than many people may have previously thought.
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 neuro-inflammatory molecules, which may contribute to the pathogenesis of numerous neurodegenerative diseases. Therefore, suppression of neuro-inflammatory 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 pro-inflammatory 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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