NDLI: Up-Regulation of Neurotrophic Factors by Cinnamon and its Metabolite Sodium Benzoate: Therapeutic Implications for Neurodegenerative Disorders

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Up-Regulation of Neurotrophic Factors by Cinnamon and its Metabolite Sodium Benzoate: Therapeutic Implications for Neurodegenerative Disorders

Journal of Neuroimmune Pharmacology : Volume 8, Issue 2, April 2013

Journal of Neuroimmune Pharmacology : Volume 8, Issue 1, March 2013

Journal of Neuroimmune Pharmacology : Volume 7

Journal of Neuroimmune Pharmacology : Volume 6

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Journal of Neuroimmune Pharmacology : Volume 4

Journal of Neuroimmune Pharmacology : Volume 3

Journal of Neuroimmune Pharmacology : Volume 2

Journal of Neuroimmune Pharmacology : Volume 1

Up-Regulation of Neurotrophic Factors by Cinnamon and its Metabolite Sodium Benzoate: Therapeutic Implications for Neurodegenerative Disorders

Content Provider	Springer Nature Link
Author	Jana, Arundhati Modi, Khushbu K. Roy, Avik Anderson, John A. Breemen, Richard B. Pahan, Kalipada
Copyright Year	2013
Abstract	This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS. NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes. Interestingly, oral administration of ground cinnamon increased the level of NaB in serum and brain and upregulated the levels of these neurotrophic factors in vivo in mouse CNS. Accordingly, oral feeding of NaB, but not NaFO, also increased the level of these neurotrophic factors in vivo in the CNS of mice. NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-κB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB. Accordingly, cinnamon feeding also increased the activity of PKA and the level of phospho-CREB in vivo in the CNS. These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA – CREB pathway, which may be of benefit for various neurodegenerative disorders.
Starting Page	739
Ending Page	755
Page Count	17
File Format	PDF
ISSN	15571890
Journal	Journal of Neuroimmune Pharmacology
Volume Number	8
Issue Number	3
e-ISSN	15571904
Language	English
Publisher	Springer US
Publisher Date	2013-03-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cinnamon Sodium benzoate Mass spectrometry BDNF NT-3 CREB Astrocytes Neurons Neurosciences Immunology Pharmacology/Toxicology Virology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Allergy Pharmacology Immunology

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