Asset Details
Do you wish to reserve the book?
Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A
Do you wish to request the book?
Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A
2019
Overview
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.
Publisher
MDPI AG,MDPI
Subject
/ Animals
/ Anti-Inflammatory Agents - pharmacology
/ Anti-Inflammatory Agents - therapeutic use
/ Humans
/ Interleukin-1beta - metabolism
/ Lipopolysaccharides - pharmacology
/ Mice
/ Parkinson Disease - immunology
/ Parkinson Disease - metabolism
/ Proteins
/ Receptors, G-Protein-Coupled - blood
/ Receptors, G-Protein-Coupled - genetics
