A Study On The Effect And Its Mechanism Of Baicalin On Mouse Hippocampus Injury After Status Epilepticus Induced By Kainic Acid

Objective This study investigated the protective effect of BCL on the mouse hippocampus neuronal cell death and Apoptosis after SE induced by KA. Methods 18 ICR male mice were randomly divided into three groups: sham group,SE group and BCL group,6 mice in each group.To established animal model of SE, 0.1μg (0.1μg/5μl) kainic acid was injectied into the intracereb- roventricular(i.c.v) of mice.To assess hippocampus injury,neuronal cell death was determined by Nissl staining and neuronal cell apoptosis was detected by TUNEL staining in hippocampus at 72h after KA injection.Results The Mean cell death scores in CA3 regions of ipsilateral hippocampus in sham group,SE group and BCL group were 1.00±0.00,4.67±1.03 and 3.00±0.89 in 72h after KA (0.1μg) administration,with significant difference (P<0.05).The mean apoptosis rates in CA1 regions of ipsilateral hippocampus in sham group,SE group and BCLgroup were 0.0000±0.0000, 0.3087±0.0344 and 0.2380±0.0300 in 72h after KA (0.1ug) administration,with significant difference(P<0.05);They were 0.0000±0.0000, 0.3607±0.0385 and 0.2956±0.0384 in CA3 regions of ipsilateral hippocampus, with significant difference(P<0.05).Conclusion Baicalin can attenuates the mouse hippocampus neuronal cell death and apoptosis after SE induced by kainic acidPart TWO The mechanism of Baicalin Attenuates the mouse hippocampus neuronal cell death and Apoptosis after SE induced by kainic acidObjective This study investigated the mechanism of baicalin attenuates the mouse hippocampus neuronal cell death and Apoptosis after SE induced by kainic acid. 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-αin 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(P<0.05).The mean levels of hippocampus IL-1βin 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(P<0.05); 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 (P<0.05);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 (P<0.05);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(P<0.05). 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 antioxidant and antiinflammatory effect.