Authors :
Presenting Author: Sukriti Kapoor, - – University of Kentucky
Rebecca Smith, PhD – University of Kentucky
Manekya Sumithrarachchi, MS – University of Kentucky
Anika Hartz, PhD – University of Kentucky
Bjoern Bauer, PhD – University of Kentucky
Rationale:
A defining characteristic of epilepsy is seizures, which release glutamate. This activates the LOX/COX signaling pathways through which inflammatory markers are released. In turn, these activate Matrix Metalloproteinases (MMPs), and MMP expression leads to a compromised blood-brain barrier, leading to more seizures. To disrupt this cycle, the goal of this study was to determine the effect of medical phytocannabainoid cannabidiol (CBD) on MMP-9 and MMP-2 expression levels. Although CBD reduces seizure burden, there is a lack of current research to support how this process works.
Methods:
In this study we used enzyme-linked immunosorbent assays (ELISA) to determine MMP-2 and MMP-9 levels in isolated rat serum from epilepsy models of five different studies: an acute epilepsy model, an acute seizure model treated with CBD, an acute epilepsy model treated with zileuton/celecoxib/CBD, a chronic epilepsy model, and a chronic epilepsy model treated with CBD. Our results show that rats treated with CBD expressed lower levels of serum MMP9 and MMP2 than untreated rats. We analyzed the results using unpaired t-tests and ANOVA tests based on the number of experimental groups used.
Results:
Statistical analysis of the ELISA results supported the hypothesis that rats treated with CBD exhibit significantly lower levels of MMP-9 and MMP-2. This study suggests that CBD treatment could have the potential to break the epileptic cycle by decreasing MMP expression, which in turn repairs barrier leakage.
Conclusions:
Our data suggest a novel approach with implications for epilepsy therapy. The results from this discovery potentially allow for a neuroprotective benefit to help epilepsy patients with a new treatment option.
Funding:
The project described was supported by grant number R01NS079507 from the National Institutes of Health/National Institute of Neurological Disorders and Stroke. The content is solely the authors’ responsibility and does not necessarily represent the official views of NINDS or the NIH.