Premium
The roles of interleukin‐1 and RhoA signaling pathway in rat epilepsy model treated with low‐frequency electrical stimulation
Author(s) -
Liu AiHua,
Wu YaTing,
Li LiPing,
Wang YuPing
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26415
Subject(s) - rhoa , epilepsy , blot , stimulation , messenger rna , signal transduction , medicine , downregulation and upregulation , chemistry , endocrinology , biology , neuroscience , microbiology and biotechnology , biochemistry , gene
This study aims to explore the correlation between interleukin‐1 (IL‐1) and epilepsy in rats when treated with low‐frequency electrical stimulation via the RhoA/ROCK signaling pathway. Twenty‐four SD rats were elected for this study, among which six rats were assigned as the normal group. And 16 rat models with epilepsy were successfully established and assigned into the model group, the ES group and the ES + IL‐8 group, with each group comprising of six rats. The seizure frequency and duration was recorded. Electroencephalogram (EEG) power was detected at α1, α2, β, θ, and δ. The mRNA expressions of IL‐1β and IL‐1R1 were detected using reverse transcription quantitative polymerase chain reaction (RT‐qPCR), and the protein expressions of RhoA, ROCK I and ROCK II were detected by western blotting. In comparison with the model group, the seizure frequency duration, the power of δ, θ, α1, α2, and β, the mRNA and protein expressions of IL‐1β and IL‐1R1, the expressions of RhoA and ROCK I proteins, and the ratio of RhoA protein between membrane and cytosol decreased in the ES group, while the expression of ROCK II increased (all P < 0.05). There was no significant difference in these indexes between the ES + IL‐8 group and the model group (all P > 0.05). These findings signified that IL‐1 might inhibit the efficacy of low‐frequency ES for epilepsy via the RhoA/ROCK signaling pathway, which may provide a theoretical basis for clinical treatment of epilepsy.