[Effects of Transcutaneous Electrostimulation of Auricular Points on Behavior and Hippocampal IL-1 β and TNF-α Expression in Temporal Lobe Epilepsy Rats].
Ključne riječi
Sažetak
OBJECTIVE
To observe the effect of transcutaneous otopoint electrostimulation (TCOES) on behavior and expression of hippocampal interleukin-1 β (IL-1 β) and tumor necrosis factor-α (TNF-α) expression in lithium-pilocarpine induced chronic spontaneous temporal lobe epilepsy (TLE) rats, so as to investigate its antiepileptic mechanism.
METHODS
Thirty-six SD rats were randomly divided into control, model and TCOES groups (n=12 in each group). The epilepsy model was established by intraperitoneal injection of lithium chloride (127.2 mg/kg), scopolamine(1 mg/kg, 20 h after the 1st injection) and pilocarpine (10 mg/kg, 30 min after scopolamine injection). Rats of the control group were treated by injection of normal saline(i.p.i.). Transcutaneous electrostimulation (1 mA, 20 Hz) was applied to bilateral otopoints "Heart" "Lung" and "Subcortex" for 20 min, once daily for 6 weeks except the weekends. The behavior reactions were observed by a video monitoring system. The expression of IL-1 β and TNF-α proteins and genes in the hippocampus were determined by immunofluorescence and quantitative real-time PCR, separately.
RESULTS
Behavioral observation showed that after TCOES intervention, the frequency of epilepsy attack was significantly decreased in comparison with pre-treatment (P<0.05). Immunofluorescence and real-time PCR showed that compared with the control group, the immunoactivity of IL-1 β and TNF-α in both hippocampal CA 1 and CA 3 regions and hippocampal IL-1 β and TNF-α gene expression were obviously increased in the model group (P<0.05, P<0.01). Following TCOES, the increased hippocampal IL-1 β and TNF-α and IL-1 β mRNA and TNF-α mRNA expression levels were all suppressed (P<0.05, P<0.01).
CONCLUSIONS
TCOES intervention has an antiepileptogenic effect in temporal lobe epilepsy rats, which may be related to its effects in down-regulating expression of proinflammatory cytokine IL-1 β and TNF-α in the hippocampus.
