Role of TLR4/NF-κB signal pathway in the hippocampus injury of status epileptic rats
- VernacularTitle:Toll样受体4/核因子-κB信号通路在癫癎持续状态大鼠海马损伤中的作用
- Author:
Qin ZHOU
;
Guangqian LI
- Publication Type:Journal Article
- Keywords:
Status epilepticus;
Hippocampus;
Receptors,cell surface;
Membrane glycopreteing;
NF-kappa B;
Signal transduction
- From:
Chinese Journal of Neurology
2008;41(10):689-694
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the expression of TLR4 and NF-κB in hippocampus injury of status epileptic rats and to study the regulating effect of PDTC on TLR4/NF-KB signal pathway and hippocampus injury, and to explore the role of TLR4/NF-κB signal pathway in the hippocampus injury of SE rats. Methods A hundred and six male Sprague-Dawley (SD) rats were randomly divided into control group (A), convulsion group (B), PDTC group (C), and group B were randomly divided into 4 subset groups (B1-B4), which would be executed at 4, 24, 48 and 72 hours after convulsion. Continuous epilepticus was induced by injecting lithium chloride and pilocarpine, and group C were daily injected with 100 mg/kg PDTC 30 minutes after convulsion stopped for 3 days. Then the histopathology changes in hippocampus were viewed by HE staining, TLR4 and NF-κB/p65 protein were detected by immunohistochemistry (IHC), the expression of TLR4 mRNA were detected by RT-PCR. Results Neuronal injury was observed after a long time of convulsion, and the change was increased gradually 72 hours after seizure, which was milder in group Cthan in group B4. The expression of TLB4 protein in group B (B1-B4 were 0.1287±0. 0260, 0. 1296± 0. 0285, 0. 1330±0. 0329 and 0. 1604±0. 0457, respectively) was significantly higher than in group A (0.0964±0.0324, t =0.0641-0.3236, all P<0.05), and that in group C (0.1271±0.0330) was much lower than in B4 group (t = -0. 0334, P <0. 01). The IHC staining of NF-κB/p65 showed that hippocampal neurons had positive expression in cell nucleus in group B compared with the group A (P < 0. 05), and the expression of NF-κB/p65 protein in group C was much lower than that in group B4 (P < 0. 01). The mRNA expression of TLB4 in rat hippocampus of group B were significantly elevated than that in group A (0. 268±0. 072, P < 0. 05), and the tendency was increased gradually, reaching the peak at 72 hours after seizure (1. 242±0. 100), and that in group C (0. 984±0. 263) was much lower than that in B4 group (t=-0.2578, P<0.01). There was a coincidence between the expression of TLB4 and NF-κB/ p65. Conclusions The increased expression of TLR4 and NF-κB/p65 in SE rat hippocampus may play an promotion role on the development of the hippocampus injury; PDTC can down regulate the expression of TLR4, and lessen the pathologic changes of hippocampus.
