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Volume 20
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10.3390/ijms20184559
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Article

Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A

by
Banabihari Giri
1,2,
Kasey Belanger
3,
Marissa Seamon
1,4,
Eric Bradley
5,
Sharad Purohit
1,6,
Raymond Chong
1,7,
John C. Morgan
1,8,
Babak Baban
9 and
Chandramohan Wakade
1,2,4,8,*
1
Charlie Norwood VA Medical Center, Augusta, GA 30904, USA
2
Department of Physical Therapy, Augusta University, Augusta, GA 30912, USA
3
Department of Physiology, Augusta University, Augusta, GA 30912, USA
4
Department of Neuroscience, Augusta University, Augusta, GA 30912, USA
5
Edward Via College of Osteopathic Medicine, Greenville, SC 29303, USA
6
Department of Undergraduate Health Professionals, Augusta University, Augusta, GA 30912, USA
7
Department of Interdisciplinary Health Sciences, Augusta University, Augusta, GA 30912, USA
8
Department of Neurology, Augusta University, Augusta, GA 30912, USA
9
Department of Oral Biology and Diagnostic Sciences, Augusta University, Augusta, GA 30912, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(18), 4559; https://doi.org/10.3390/ijms20184559
Received: 14 August 2019 / Revised: 6 September 2019 / Accepted: 10 September 2019 / Published: 14 September 2019
(This article belongs to the Section Molecular Immunology)
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Abstract

In this study, we used macrophage RAW264.7 cells to elucidate the molecular mechanism underlying the anti-inflammatory actions of niacin. Anti-inflammatory actions of niacin and a possible role of its receptor GPR109A have been studied previously. However, the precise molecular mechanism of niacin’s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-κB) induced by lipopolysaccharide (LPS) in the nucleus of RAW264.7 cells. The reduction in the nuclear translocation in turn decreased the expression of pro-inflammatory cytokines IL-1β, IL-6 in RAW264.7 cells. We observed a decrease in the nuclear translocation of p-NF-κB and the expression of inflammatory cytokines after knockdown of GPR109A in RAW264.7 cells. Our results suggest that these molecular actions of niacin are mediated via its receptor GPR109A (also known as HCAR2) by controlling the translocation of p-NF-κB to the nucleus. Overall, our findings suggest that niacin treatment may have potential in reducing inflammation by targeting GPR109A. View Full-Text
Keywords: niacin; vitamin B3; GPR109A; macrophage; lipopolysaccharide; neuroinflammation; cytokine; neurodegenerative disease; Parkinson’s disease niacin; vitamin B3; GPR109A; macrophage; lipopolysaccharide; neuroinflammation; cytokine; neurodegenerative disease; Parkinson’s disease
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MDPI and ACS Style

Giri, B.; Belanger, K.; Seamon, M.; Bradley, E.; Purohit, S.; Chong, R.; Morgan, J.C.; Baban, B.; Wakade, C. Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A. Int. J. Mol. Sci. 2019, 20, 4559. https://doi.org/10.3390/ijms20184559

AMA Style

Giri B, Belanger K, Seamon M, Bradley E, Purohit S, Chong R, Morgan JC, Baban B, Wakade C. Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A. International Journal of Molecular Sciences. 2019; 20(18):4559. https://doi.org/10.3390/ijms20184559

Chicago/Turabian Style

Giri, Banabihari, Kasey Belanger, Marissa Seamon, Eric Bradley, Sharad Purohit, Raymond Chong, John C. Morgan, Babak Baban, and Chandramohan Wakade. 2019. "Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A" International Journal of Molecular Sciences 20, no. 18: 4559. https://doi.org/10.3390/ijms20184559

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