Cocaine Causes Cell Death and Activates NF-κB in PC12 Cells
Author Information
Author(s): Lucilia B Lepsch, Carolina D Munhoz, Elisa M Kawamoto, Lidia M Yshii, Larissa S Lima, Maria F Curi-Boaventura, Thais ML Salgado, Rui Curi, Cleopatra S Planeta, Cristoforo Scavone
Primary Institution: University of São Paulo
Hypothesis
Does cocaine induce cell death and activate NF-κB in PC12 cells?
Conclusion
Cocaine exposure leads to cell death and activates NF-κB in PC12 cells, with the activation being partially mediated by D1 receptors.
Supporting Evidence
- Cocaine treatment induced DNA fragmentation and cellular membrane rupture in PC12 cells.
- Activation of caspase-3 was observed after cocaine treatment.
- Cocaine reduced Bcl-2 protein levels, which is associated with increased apoptosis.
- Nuclear factor kappa-B (NF-κB) was activated in response to cocaine treatment.
- Pre-treatment with a D1 receptor antagonist reduced NF-κB activation.
- Inhibition of NF-κB increased cell death caused by cocaine.
- Cocaine exposure led to increased LDH release, indicating cell membrane damage.
- BDNF mRNA levels transiently increased after cocaine treatment.
Takeaway
Cocaine can harm brain cells and make them die, and it does this by turning on a special protein that usually helps protect cells.
Methodology
PC12 cells were treated with cocaine and various inhibitors, and cell death was assessed using flow cytometry, MTT, and LDH assays.
Limitations
The study primarily focuses on in vitro results, which may not fully represent in vivo conditions.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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