马桑内酯致大鼠癫痫持续状态后海马神经细胞凋亡的观察

A study of apoptosis of the hippocampus cells after status epilepticus of rats induced by coraria lactone

观察马桑内酯（ｃｏｒｉａｒｉａｌａｃｔｏｎｅ，ＣＬ）诱导鼠癫痫持续状态（ＳＥ）时海马细胞中ＤＮＡ损伤及凋亡现象。方法用流式细胞术检测海马细胞中ＤＮＡ状态，用免疫组织化学方法显示海马谷氨酸阳性细胞，并以流式细胞术免疫荧光法测定海马细胞中ＢＣＬ－２样蛋白含量。结果ＳＥ后海马细胞中有ＤＮＡ损伤断裂；海马ＣＡ３区谷氨酸阳性细胞数量减少，着色变淡；海马细胞中ＢＣＬ－２样蛋白增加。结论ＳＥ可诱导海马细胞ＤＮＡ损伤进而凋亡；ＳＥ时谷氨酸过量释放可造成突触后靶细胞损伤。ＢＣＬ－２样蛋白增加可能是ＢＣＬ－２家族蛋白共同变化的结果，是细胞自身的保护机制，以抗损伤和凋亡。

Objective As the selective neuronal vulnerability had been a feature of various types of epilepsy, the purpose of our study was to investigate the DNA damage and apoptosis of the hippocampus cells in the models of stuatus epilepticus (SE) of the rats induced by coriaria lactone (CL). Method DNA in the hippocampus cells was measured with flow cytomety. With the immunohistochemical study, the glutaic acid energy neurons were shown in the hippocampus. The quatitaties of the substance like the BCL 2 protein in the hippocampus cells were demtermined with the flow cytometry and immunofluorescence techniques. There were features of the apoptosis from damaged DNA into fragmentations and increased substance like BCL 2 protein in the hippocampus cells after SE. Results The descrease of the glutamic acid energy neurons was shown in the hippocampal areas of CA 3 with poor staining. Conclusion SE could cause DNA damage, inducing apoptosis of the hippocampus cells. Releasing of excessive amounts of glutamic acid in SE, if severe enough, might result in an injury of the postsynaptic target cells. An increase of the substance like BCL 2 portein in the cells might indicate a simultaneous change of the whole BCL 2 family of proteins in order to render a cellular self protection of the involved cells from being injured and apoptosed.