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目的探讨海人藻酸致急慢性癫痫模型中Nrf2的变化及其对神经元的影响。方法大鼠海马内注射浓度为(1μg/μl)海人藻酸(KA)1.0μl后,随机分为模型24 h组(急性模型组)及模型28 d组(慢性模型组),假手术组注射等体积的生理盐水,每组10只。尼氏染色法观察神经元的变化;免疫组化及免疫印迹法测定Nrf2的表达。结果尼氏染色结果显示,与假手术组相比,模型24 h组与模型28 d组尼氏小体均减少,但以模型28 d组减少显著;免疫组化及免疫印迹结果表明,模型24 h组的表达增加,模型28 d组表达则减少。结论 Nrf2在急性模型表达上调,具有抗氧化作用,进而保护神经元;慢性模型中则不具有抗氧化作用,神经元受损。
Objective To investigate the changes of Nrf2 in acute and chronic epilepsy induced by kainic acid and its effect on neurons. Methods Rat hippocampus was injected intraperitoneally with 1.0μl of kainic acid (KA) (1μg / μl) and then randomly divided into 24 hours group (acute model group), 28 days model group (chronic model group), sham operation group Injection of equal volume of saline, 10 per group. Nissl staining was used to observe the changes of neurons. Immunohistochemistry and Western blotting were used to detect the expression of Nrf2. Results Nissl staining showed that compared with the sham-operation group, Nissl body decreased in 24 h group and 28 d group, but decreased significantly in 28 d group. Immunohistochemistry and Western blotting showed that model 24 h group increased expression of the model 28 d group decreased expression. Conclusion Nrf2 is upregulated in acute model and has anti-oxidant effect, which can protect neurons. In chronic model, Nrf2 does not have anti-oxidant effect and neurons are impaired.