| Objective: In the past few years, cell cycle inhibition plays an important role in thetreatment of tumors. Additionally, a series of central nervous system (CNS) diseasessuch as spinal cord injury (SCI), stroke, and Parkinson’s disease (PD), show someresponses to cyclin-dependent kinase (CDK) inhibitors. However, whether cell cycleinhibition has an effect or not on epilepsy is still unknown. This study aimed toinvestigate the relationship between cell cycle inhibition and Temporal Lobe Epilepsy.Methods: In this study, we investigated the correlation between temporal lobeepilepsy (TLE) and cell cycle inhibition through pilocarpine-induced rat models oftemporal lobe epilepsy and surgical samples of temporal neocortex from intractableepilepsy patients. Olomoucine (a CDK inhibitor) was used at an acute stage ofinduced TLE. Behavioral changes and electroencephalogram (EEG) were interpretedafter intervention. We also used immunohistochemistry (IHC) to detect the expressionof glial fibrillary acidic protein (GFAP) and adenosine kinase (ADK). Results: We found that the frequency of seizures and the expression of GFAP andADK were attenuated in olomoucine-treated group. What’s more, compared withnon-epileptic human brain tissue, the expression of ADK was significantly increasedin the epileptic human brain.Conclusion: The present results suggested that certain cell cycle inhibition mayimprove epilepsy to some extent by inhibiting astrogliosis and the subsequent overexpression of ADK. Our paper also suggests that astrocyte-specific cell cycleinhibition may be considered as a promising therapeutic intervention for epilepsy. |