Abstract
OBJECTIVE: To explore the molecular mechanism of neuropathologic damage induced by radiofrequency ablation at different temperatures. METHODS: This is basic research, and 36 SD rats were used to construct the neuropathological injury model. The rats were subjected to radiofrequency stimulation at different temperatures and were divided into 6 groups according to the temperature injury: 42°, 47°, 52°, 57°, 62°, and 67°C groups. Conduction time, conduction distance, and nerve conduction velocity were recorded after temperature injury. HE-staining was used to observe the histopathological morphology of the sciatic nerve. The expression of SCN9A, SCN3B, and NFASC protein in sciatic nerve tissue were detected by western blot. RESULTS: With the increase in temperature, nerve conduction velocity gradually decreased, and neurons were damaged when the temperature was 67°C. HE-staining showed that the degrees of degeneration of neurons in rats at 47°, 52°, 57°, 62°, and 67°C were gradually increased. The expression of SCN9A, SCN3B protein in 57°, 62°, 67°C groups were much higher than that of NC, 42°, 47°, 52°C groups. However, the expression of NFASC protein in 57°, 62°, 67°C groups was much lower than that of the NC, 42°, 47°, 52°C groups. CONCLUSION: There was a positive correlation between temperature caused by the radiofrequency stimulation to neuropathological damage. The mechanism is closely related to the expression of SCN9A, SCN3B, and NFASC protein in nerve tissue caused by heat transfer injury.