|Qin, Bolin -|
|Panickar, Kiran -|
Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 2, 2013
Publication Date: November 12, 2013
Citation: Qin, B., Panickar, K., Anderson, R.A. 2013. Cinnamon polyphenols regulate S100ß, sirtuins, and neuroactive proteins in rat C6 glioma cells. Journal of Nutrition. 30(2):210-217. Interpretive Summary: Dietary polyphenols exert protective effects in a variety of brain disorders, including Alzheimer’s disease, ischemia/stroke, and Parkinson’s disease. The cause of these diseases may be related to decreased function of insulin and increased inflammation, which are improved by polyphenols, particularly those found in cinnamon. The objective of this study was to investigate the effects of an aqueous extract of cinnamon, high in polyphenols, on brain cells ( rat C6 glioma cells). Cinnamon polyphenols significantly enhanced S100ß, a Ca2+-binding protein, and also enhanced protein levels of sirtuin 1, 2, and 3, which are important in cell survival and longevity. Overall, these results suggest that cinnamon polyphenols may contribute to the function and survival of normal brain cells and the prevention of brain disorders including Alzheimer’s and related diseases. This work should be of benefit to scientists studying the effects of diet on overall brain function as well as the lay public.
Technical Abstract: Dietary polyphenols exert neuroprotective effects in a variety of brain disorders, including Alzheimer’s disease, ischemia/stroke, and Parkinson’s disease. The protective effects of polyphenols in the brain and in neural cell cultures have been established. The role of glial cells in providing protective effects to neurons is also known. However, the effects of polyphenols on molecular targets in glial cells that underlie the protective effects of such cells are scarce. The objective of this study was to investigate the effects of an aqueous extract of cinnamon, high in polyphenols (CP), in rat C6 glioma cells. CP significantly enhanced secretion of S100ß, a Ca2+-binding protein, and increased intracellular S100ß expression as determined by immunoprecitation/ immunoblotting and immunofluorescence imaging after 24 h of incubation. CP also enhanced protein levels of sirtuin 1, 2, and 3, deacetylases important in cell survival, and the tumor suppressor protein, p53, and inhibited the inflammatory factors, TNF-a, and phospho-p65, a subunit of NF'B. CP also up regulated levels of phospho-p38, ERK and MAPKAPK2 kinases that may be important for pro-survival functions . Overall, these results suggest that the effects of CP on upregulating pro-survival proteins, activating MAPK pathways, and decreasing pro-inflammatory cytokines may contribute to their neuroprotective effects.