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目的研究氯化锂-匹鲁卡品癫痫持续状态(SE)大鼠模型中海马神经元蛋白激酶Cδ亚型(PKCδ)的表达及他克莫司(FK506)对其的影响。方法将108只健康成年雄性大鼠随机分为对照组、癫痫组和FK506处理组,每组36只。采用HE染色法观察大鼠癫痫持续状态(SE)后海马神经元的损伤,应用逆转录PCR、免疫组织化学法检测各组大鼠海马PKCδmRNA及蛋白的表达。结果对照组PKCδmRNA和蛋白仅有少量表达;与对照组相比,癫痫组各个时点PKCδ表达均显著增多(P<0.05),SE后6 h PKCδmRNA表达最高,PKCδ蛋白的平均光密度值SE后12 h达高峰(P<0.01),以后二者均逐渐降低,但72 h仍高于对照组水平(P<0.05);FK506预处理可降低其表达,同时可减轻海马神经元损伤(P<0.05)。结论 FK506可能通过抑制依赖PKCδ的细胞凋亡途径,发挥抗癫痫和脑保护作用。
Objective To investigate the expression of protein kinase Cδ subtype (PKCδ) of hippocampus neurons in lithium chloride-pilocarpine (SE) rat model and the effect of FK506 on it. Methods 108 healthy adult male rats were randomly divided into control group, epilepsy group and FK506 treatment group, 36 rats in each group. The damage of hippocampal neurons after epileptic seizure (SE) in rats was observed by HE staining. The expression of PKCδmRNA and protein in hippocampus of hippocampus were detected by RT-PCR and immunohistochemistry. Results Compared with the control group, the expression of PKCδmRNA and protein in the control group was significantly increased (P <0.05), and the expression of PKCδmRNA at 6h after SE was the highest (P <0.01). Afterwards, both of them decreased gradually, but were still higher than those of the control group at 72 h (P <0.05). FK506 preconditioning reduced the expression of neurons and decreased the neuronal damage in hippocampus (P < 0.05). Conclusion FK506 may play an antiepileptic and brain protective role by inhibiting the apoptosis-dependent PKCδ-dependent pathways.