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Published on: June 16, 2023
[Brain injury in adenosine A1 receptor knock-out mice after pentetrazole kindling and its correlation with COX-2]
Hui-cong Kang1, Feng Xu, Xiao-yan Liu
1Neurology Department of Tongji Hospital Affiliated to Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China.
Objective:
To investigate the brain injury of neurocytes in hippocampus of adenosine A1 receptor knock-out mice during pentetrazole kindling and detect the correlation of brain injury and the expression of COX-2 so as to evaluate the neuroprotective function of adenosine A1 receptor and its mechanism.
Methods:
The animals were divided into two groups: wild type group and KO group. The kindling model was established by injection of pentetrazole into abdominal cavity. The expression of brain injury related protein, caspase-3 and COX-2 in hippocampus was investigated separately at different time points (24 hour, 1 month) post-kindling.
Results:
The expression of Caspase-3 and COX-2 increased in KO group both during acute and chronic phases post-kindling compared with normal mice. There was statistical difference (P < 0.05). Furthermore, the expression levels of two proteins were higher at 1 month compared with 24 hour (P < 0.01). These results indicated that the increased expression of Caspase-3 and COX-2 post-kindling was earlier and much more in KO mice as compared with wild-type ones.
Conclusion:
Adenosine exerts strong neuroprotective functions through the activation of adenosine A1 receptor. This receptor reduces cell apoptosis during pentetrazole kindling. Cyclooxygenase-2 (COX-2) reflects the extent of brain injury. The neuroprotective function mediated by adenosine A1 receptor might be related with COX-2.
