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目的观察大鼠癫痫持续状态(Status epilepticus,SE)后海马组织脑红蛋白(Neuroglobin,NGB)表达动态变化,探讨NGB在癫痫发作中的作用。方法健康成年雄性SpragueDawley大鼠40只,随机分为对照组(n=5)、癫痫模型实验组(n=35);实验组再依据观察时间分为:0、1、3、12、24 h和10、30 d。应用锂-匹罗卡品(20~127 mg/kg)建立大鼠SE模型,观察大鼠致痫期间行为学变化;采用尼氏(Nissl)染色检测海马组织神经元损伤情况;SABC免疫组化法检测海马组织NGB表达水平。结果 SE后,海马组织各区均出现不同程度神经元细胞损伤坏死,随着发作时程进展,CA1、CA3区存活神经元呈近直线下降趋势。其中CA1区(12、24 h,10、30d)、CA3区(0、12、24 h,10、30 d)和(DG区12、24 h,10、30 d)神经元存活数较对照组明显减少(P<0.05)。大鼠SE后,海马各区NGB表达水平均上调,CA1、DG区NGB表达均于SE后24 h达顶峰后轻度下降,但仍持续高于对照组,CA3区NGB表达呈持续升高趋势。其中CA1区(24 h,10、30 d)、CA3区(24 h,10、30 d)和DG区(12、24 h,10、30 d)NGB表达水平均较对照组显著升高(P<0.05)。另外,海马CA1和CA3区神经元存活数与NGB表达水平呈正相关(R=0.206,P=0.015;R=0.306,P=0.011)。结论大鼠SE后海马各区NGB表达上调,且与CA1、CA3区神经元存活数呈正相关,提示NGB表达上调可能是癫痫发作所致缺血缺氧损害的一种代偿保护机制,参与癫痫相关神经元损害的保护。
Objective To observe the dynamic changes of neuroglobin (NGB) expression in hippocampus after status epilepticus (SE) in rats and to explore the role of NGB in seizures. Methods Forty healthy adult male Sprague Dawley rats were randomly divided into control group (n = 5) and epilepsy model group (n = 35). The experimental group was divided into two groups according to observation time: 0, 1, 3, 12, 24 h And 10,30 d. SE model was established by lithium-pilocarpine (20-127 mg / kg) to observe the changes of behavior during the epileptic seizure in rats. Nissl staining was used to detect neuronal damage in hippocampus. SABC immunohistochemistry Method to detect the expression of NGB in hippocampus. Results After SE, different degrees of neuronal cell necrosis appeared in the hippocampus, and the neurons in the CA1 and CA3 areas showed a nearly straight downward trend with the progression of the attack. The survival rate of neurons in CA1 area (12,24 h, 10,30 d), CA3 area (0,12,24 h, 10,30 d) and (DG area 12,24 h, 10,30 d) Significantly reduced (P <0.05). After SE, the expression of NGB in hippocampus was up-regulated. The expression of NGB in CA1 and DG decreased slightly at 24 h after SE, but remained higher than that in control group. The expression of NGB in CA3 continued to increase. The expression level of NGB in CA1 area (24 h, 10,30 d), CA3 area (24 h, 10,30 d) and DG area (12,24 h, 10,30 d) were significantly higher than those in control group (P <0.05). In addition, neuronal survival numbers in CA1 and CA3 hippocampus were positively correlated with NGB expression (R = 0.206, P = 0.015; R = 0.306, P = 0.011). Conclusions The expression of NGB in hippocampus of rats after SE is up-regulated, and it is positively correlated with the number of neurons in CA1 and CA3 area. It suggests that the up-regulation of NGB may be a compensatory mechanism of protection against ischemia-hypoxia induced by seizures and is involved in epilepsy-related Protection of neuronal damage.