摘要
目的探讨黄芩苷对海人酸诱导的小鼠癫痫持续状态后海马神经细胞凋亡的影响。方法 54只ICR雄性小鼠随机分为对照组、癫痫持续状态(SE)组、黄芩苷治疗组(100mg/kg)。采用腹腔内注入海人酸(12mg/kg)建立小鼠癫痫持续状态模型。通过TUNEL染色观察小鼠海马CA1、CA3区神经细胞的凋亡程度;免疫组化观察海马组织中caspase-3细胞的阳性表达情况;RT-PCR检测海马组织中Bax、Bcl-2 mRNA的含量;Western blot检测Bax、Bcl-2和caspase-3蛋白的表达量。结果与癫痫持续状态组相比,黄芩苷可显著减轻癫痫持续状态后海马神经细胞的凋亡(CA1区:0.3984±0.0586 vs.0.7258±0.0235,P<0.05;CA3区:0.3593±0.0391 vs.0.6191±0.0686,P<0.05),降低海马中Bax mRNA的合成和Bax、caspase-3蛋白的表达(P<0.05),增加Bcl-2 mRNA及蛋白的表达(P<0.05)。结论黄芩苷能够减轻小鼠癫痫持续状态后海马神经细胞的凋亡,其作用机制可能通过上调Bcl-2的表达和下调Bax、caspase-3的表达来发挥抗凋亡作用。
Objective To explore the effects of baicalin on the apoptosis of the hippocampal neurons after status epilepticus in mice induced by kainic acid. Methods Fifth-four ICR male mice were randomly divided into three groups ： control group, SE group and baicalin group. Baicalin was administered at 100mg/kg. Status epilepticus was induced by intraperitoneal injection of 12mg/kg kainic acid in mice. TUNEL staining was used to determine neuron apoptosis in the hippocampus CA1 and CA3 areas. Immunohistochemistry was used to examine the expression of caspase-3. Reverse transcription polymerase chain reaction （RT-PCR） were used to detect the mRNA expression of Bax and Bcl-2 . Western blot were used to detect the protein expression of Bax, Bcl-2 and caspase-3. Results Baicalin significantly attenuated the apoptosis of the hippocampal neurons after status epilepticus in mice （P〈0.05）. In addition, Baicalin decreased the mRNA expression of Bax and inhibited the protein expression of Bax and caspase-3 （P〈0.05） whereas increased the mRNA and protein expression of Bcl-2 （P〈0.05）. Conclusions Baicalin decreases epilepticus-induced hippocampal neuron apoptosis possibly through upregnlation of Bcl-2 and downregulation of Bax and caspase-3.
出处
《中国神经精神疾病杂志》
CAS
CSCD
北大核心
2014年第5期269-274,共6页
Chinese Journal of Nervous and Mental Diseases
关键词
癫痫
黄芩苷
海人酸
凋亡
Epilepsy Baicalin Kainic acid Apoptosis
