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Published on: July 20, 2019
Nicotinamide prevents apoptosis in human cortical neuronal cells
Suraj G Bhansali1, Daniel A Brazeau, Manisha Sonee
1College of Pharmacy, South Dakota State University, Brookings, South Dakota, USA.
Toxicology Mechanisms and Methods
|December 22, 2009
Summary
Nicotinamide prevents neuronal cell death caused by t-BuOOH by inhibiting apoptosis. This neuroprotective effect involves regulating apoptosis-related genes, including inhibitors of apoptosis (IAPs).
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Tertiary butylhydroperoxide (t-BuOOH) induces cell death in human cortical neuronal cells (HCN2).
- Poly (ADP-ribose) polymerase (PARP) inhibitor nicotinamide previously showed neuroprotective effects against t-BuOOH.
- Apoptosis, indicated by TUNEL-positive cells, occurs 6 hours after t-BuOOH exposure.
Purpose of the Study:
- To investigate the neuroprotective mechanisms of nicotinamide against t-BuOOH-induced neuronal cell death.
- To analyze the effects of nicotinamide on apoptosis-related gene expression in HCN2 cells.
- To elucidate how nicotinamide regulates apoptotic pathways.
Main Methods:
- Human cortical neuronal cells (HCN2) were treated with t-BuOOH and/or nicotinamide.
- Apoptosis was assessed using TUNEL assays.
- DNA microarray analysis was performed to examine gene expression profiles.
Main Results:
- t-BuOOH induced apoptosis and upregulated proapoptotic genes (ICH-2, BimL).
- Nicotinamide pretreatment prevented cell death and apoptosis.
- Nicotinamide upregulated inhibitors of apoptosis (IAP) genes and other genes like glyceraldehydes-3-phosphate dehydrogenase, p75TNFR, TRAIL2, TNFR1, and HVEM-L.
Conclusions:
- Nicotinamide confers neuroprotection against t-BuOOH by inhibiting apoptosis.
- Elevating IAP gene expression is a key mechanism for nicotinamide's neuroprotective action.
- Nicotinamide modulates multiple apoptosis-related genes, demonstrating a complex regulatory role in neuronal cell survival.
