目的 观察热性惊厥(FS)幼鼠海马神经细胞凋亡数变化,为探讨幼鼠FS脑损伤机制及寻求有效的防治措施提供理论依据.方法 按析因设计,64只14日龄SD幼鼠随机均分为4组(n=16),即对照组:生理盐水(NS)组;试验组:脂多糖(LPS)+海人藻酸(KA)组;KA组;LPS组.采用LPS联合低剂量KA腹腔注射的方法诱导幼鼠FS.H-E染色观察幼鼠海马神经元显微结构的改变,TUNEL法检测海马神经细胞凋亡数的变化.结果 LPS+KA组16只幼鼠均出现FS,发作时肛温为(39.3±0.4)℃;其他组幼鼠均未出现FS.LPS+KA组、LPS组、KA组及NS组幼鼠末次腹腔注射后24 h,海马CA1区神经细胞凋亡数分别为(20.63±3.78),(11.63±3.58),(4.06±2.86)及(3.06±2.01),48 h分别为(20.63±1.69),(12.25±3.62),(5.50±3.06)及(3.19±1.98).FS持续时间与海马细胞凋亡程度呈正相关(r=0.866,P＜0.01).结论 LPS联合低剂量KA腹腔注射诱导FS可导致幼鼠海马神经细胞损伤.%Objective To observe the changes of apoptosis in rat hippocampal neurons induced by febrile seizures (FS) , and to provide the theoretical basis for exploring the brain damage of FS and the effective prevention and control measures. Methods Factorial experiment design was: sixty-four M-day-old Sprague-Dawley(SD) rats were randomly divided into four groups(n=16): Control group: normal so-dium(NS)group; Experimental group: Lipopolysaccharide(LPS) and Low-dose Kainic Acid(KA) group; KA group; LPS group. FS was induced by intraperitoneal injection of LPS combined with low-dose KA. Then the histopathology changes in hippocampus were viewed by H-E staining, and the number of apoptosis nerve cells in the hippocampus was observed by TdT-mediated dUTP nick end labeling (TUNEL). Results Sixteen rats all appeared seizures in LPS+KA group, and the average rectal temperature of seizures was (39. 3 + 0. 4)°C ;While rats in other groups did not appear FS. After 24 h of the last intraperitoneal injection, the numbers of neuronal apoptosis in the hippocampus of LPS + KA, LPS, KA, NS groups were (20. 63 + 3. 78), (11.63 + 3.58), (4.06 + 2.86), (3.06 + 2.01) respectively. The numbers after 48 h were (20. 63 + 1. 69), (12.25 + 3.62), (5.50 + 3.06), (3. 19 + 1. 98) respectively. The duration of FS was positively correlated with the degree of hippocampal apoptosis (r=0. 866, P<0. 01). Conclusions FS induced by intraperitoneal injection of LPS combined with low-dose KA can lead to damage of nerve cells in hippocampus.
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