黄芩苷对海人酸诱导小鼠癫痫持续状态后海马损伤的影响及机制分析-外科学(神经外科学)专业毕业论文.docxVIP

福建医科大学 福建医科大学 2011 届硕士研究生毕业论文 8 8 Methods：54 ICR male mice were randomly divided into three groups：sham group， SE group and BCL group,18 mice in each group．To established animal model of SE,0.1μg(0.1μg/5μl) kainic acid was injectied into the intracerebroventricular(i.c.v) of mice．The expression of GSH, MDA and the SOD activity was detected by Spectrophotometry, the level of TNF-αand IL-1βwas examined by ELISA in 6 mice hippocampus every group at 24h after KA injection.The activations of microglia and astrocytes were analyzed by immunohistochemistry using anti-Iba-1 and anti-GFAP antibodies in 6 mice hippocampus every group at 72h after KA injection. Results The mean levels of hippocampus TNF-α in sham group,SE group and BCL group were 757.85±75.65 (pm/mg),1168.83±70.53(pm/mg6) and 951.23± 116.41(pm/mg) in 24h after KA administration,with significant difference(P0.05).The mean levels of hippocampus IL-1β in sham group,SE group and BCL group were1466.42±89.77(pm/mg),3401.77±190.88(pm/mg) and 2567.87 ± 165.68(pm/mg),with significant difference(P0.05); the mean levels of hippocampus GSH in sham group,SE group and BCL group were 17.51 ± 1.94(nm/mg),10.63 ± 1.58(nm/mg) and 13.78 ± 2.45(nm/mg), with significant difference (P0.05)；the mean levels of hippocampus MDA in sham group,SE group and BCL group were 273.47±28.33(nm/mg),627.39±65.04(nm/mg) and 495.86± 68.28(nm/mg),with significant difference (P0.05) ； the mean SOD activity of hippocampus in sham group,SE group and BCL group were 58.62±4.36 (mu/mg), 32.65±5.27(mu/mg) and 42.81±6.72(mu/mg),with significant difference(P0.05). Kainic acid caused an increase of the number and cell bodies of microglia and astrocytes in the mouse hippocampus.Baicalin treatment can suppressive the increase of the number and cell bodies of microglia and astrocytes induced by kainic acid. Conclusion Baicalin may attenuates the mouse hippocampus neuronal cell death and apoptosis after SE induced by kainic acid through antiox