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目的研究白细胞介素2(IL-2)致痫与蛋白酪氨酸激酶(Jak)/信号转导子和转录激活子(Stats)信号转导途径的关系。方法用免疫细胞化学方法研究IL-2致痫大鼠脑内蛋白酪氨酸激酶Jak1的表达变化,及预先应用Jak1抑制剂和糖皮质激素干预后,再用IL-2致痫后脑内N-甲基-D-天门冬氨酸型受体-1(NMDAR-1)和谷氨酸(Glu)的表达变化。结果侧脑室注射IL-2后大鼠出现明显的癫痫发作,其Jak1的表达较对照组明显增强(P<0.01),免疫抑制剂环孢霉素可部分抑制此效应;Jak1抑制剂植物异黄酮和免疫抑制剂糖皮质激素可明显抑制IL-2致痫大鼠的癫痫行为,其NMDAR-1和Glu的表达较IL-2组显著降低(P<0.05)。结论在IL-2致痫中,Jak1在其信号转导途径中发挥重要作用。
Objective To investigate the relationship between interleukin 2 (IL-2) -deletion and protein tyrosine kinase (Jak) / signal transducers and activators of transcription (STAT) signal transduction pathway. Methods Immunocytochemistry was used to study the expression of protein tyrosine kinase Jak1 in the brain of IL-2-induced epilepsy rats. After pretreatment with Jak1 inhibitor and glucocorticoid, the levels of N- Methyl-D-aspartate receptor-1 (NMDAR-1) and glutamate (Glu). Results After intracerebroventricular injection of IL-2, there was a significant seizure in rats. The expression of Jak1 was significantly increased compared with the control group (P <0.01). Cyclosporine immunosuppressant could partially inhibit this effect. Jak1 inhibitor plant isoflavone And immunosuppressant glucocorticoids could significantly inhibit the epileptic behavior of epilepsy rats induced by IL-2, the expression of NMDAR-1 and Glu was significantly lower than that of IL-2 group (P <0.05). Conclusions In IL-2-induced epilepsy, Jak1 plays an important role in its signal transduction pathway.