MECHANISM OF HIPPOCAMPAL CD95/CD95L AND BDNF/TRKB PATHWAY IN THE DEVELOPMENT OF TRIGEMINAL NEURALGIA IN RATS

Ruyun Deng

Department of Anesthesia Surgery, Daqing Oilfield General Hospital, Daqing, 163000, China

Objective: This study aims to explore the mechanism of hippocampal apoptotic factor CD95 and its ligand (CD95L) pathway, as well as brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) pathway, in the development of trigeminal neuralgia in rats. 

Methods: Forty healthy adult male SD rats were randomly divided into control and model groups. The model group was used to establish the trigeminal neuralgia model, while the control group was exposed to the infraorbital nerve without ligation. The mechanical pain domain was measured before the operation, 5 days after the operation, 15 days after the operation, and 30 days after the operation. The learning and memory function of rats was evaluated by a water maze test 30 days after modeling. The relative expression levels of interleukin-1β (IL-1 β), Caspase-3, BDNF, TrkB, CD95, and CD95L were detected by Western blot. 

Results: There was no significant difference in mechanical pain area between the two groups before operation (P>0.05). The mechanical pain area of the model group was significantly lower than that of the control group at 5, 15, and 30 days after the operation (P<0.05). The escape latency level of the model group was significantly higher than that of the control group (P<0.05). The times of crossing the platform and the percentage of time in the target quadrant in the model group were significantly lower than those in the control group (P<0.05). IL-1 in model group β The protein levels of Caspase-3 and Caspase-3 in the treatment group were significantly higher than those in the control group (P<0.05). The protein levels of BDNF and TrkB in the model group were significantly lower than those in the control group (P<0.05). The protein levels of CD95 and CD95L in the model group were significantly higher than those in the control group (P<0.05). 

Conclusion: Hippocampal CD95/CD95L and BDNF/TrkB pathways mediate the trigeminal neuralgia occurrence and development in rats by regulating neuroinflammation and neuronal apoptosis and even leading to cognitive impairment in rats.