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

Autor: Babak Baban, John C. Morgan, Kasey Belanger, Chandramohan G. Wakade, Banabihari Giri, Marissa Seamon, Sharad Purohit, Raymond K.Y. Chong, Eric Bradley
Rok vydání: 2019
Předmět:
Lipopolysaccharides
Lipopolysaccharide
medicine.medical_treatment
Interleukin-1beta
Anti-Inflammatory Agents
Chromosomal translocation
niacin
Pharmacology
vitamin B3
Receptors
G-Protein-Coupled
neuroinflammation
lcsh:Chemistry
chemistry.chemical_compound
Mice
0302 clinical medicine
neurodegenerative disease
cytokine
Receptor
lcsh:QH301-705.5
Spectroscopy
0303 health sciences
Mice
Inbred BALB C
Chemistry
digestive
oral
and skin physiology
lipopolysaccharide
NF-kappa B
food and beverages
Parkinson Disease
General Medicine
3. Good health
Computer Science Applications
Cytokine
medicine.symptom
Niacin
Inflammation
macrophage
Catalysis
Article
Proinflammatory cytokine
Inorganic Chemistry
03 medical and health sciences
medicine
Animals
Humans
Physical and Theoretical Chemistry
Molecular Biology
Neuroinflammation
030304 developmental biology
Interleukin-6
Macrophages
Organic Chemistry
nutritional and metabolic diseases
GPR109A
RAW 264.7 Cells
lcsh:Biology (General)
lcsh:QD1-999
Parkinson’s disease
030217 neurology & neurosurgery
Zdroj: International Journal of Molecular Sciences
International Journal of Molecular Sciences, Vol 20, Iss 18, p 4559 (2019)
Volume 20
Issue 18
ISSN: 1422-0067
Popis: 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&rsquo
s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-&kappa
B) 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-1&beta
IL-6 in RAW264.7 cells. We observed a decrease in the nuclear translocation of p-NF-&kappa
B 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-&kappa
B to the nucleus. Overall, our findings suggest that niacin treatment may have potential in reducing inflammation by targeting GPR109A.
Databáze: OpenAIRE
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