中文摘要：

目的比较惊厥持续状态（SC）后不同年龄大鼠海马凋亡调控基因bcl-2和c-Jun表达的变化,探索未成熟脑耐受惊厥性脑损伤的分子基础。方法制作幼年和成年Wistar大鼠SC模型,同时设置正常对照组和实验对照组,每组8只。于SC后3 h,6 h,12 h,1 d,3 d和7 d分别处死动物,免疫组化、原位杂交和RT-PCR测定海马bcl-2和c-Jun蛋白及mRNA的表达。结果 SC后幼年组和成年组海马c-Jun蛋白表达均升高,SC后6 h达高峰,显著高于正常对照组（P〈0.01）,12 h后开始回落。幼年SC组c-Jun蛋白表达于SC后1 d已降至幼年正常对照组水平,而成年SC组直至SC后7 d仍显著高于成年正常对照组（P〈0.05）。SC后6 h,12 h,1 d,3 d和7 d成年SC组c-Jun蛋白表达均显著高于幼年SC组（P〈0.05）。SC后幼年组和成年组海马c-Jun mRNA的表达与其蛋白表达规律类似。SC后幼年组和成年组海马bcl-2蛋白及mRNA表达升高不明显。结论 SC诱导海马凋亡促进基因c-Jun表达增高,幼年鼠较成年鼠表达明显为弱,且持续时间短,这可能是未成熟脑抵抗惊厥性脑损伤的机制之一。SC未能明显诱发凋亡抑制基因bcl-2的强表达,其表达受年龄影响小。

英文摘要：

Objective To explore the molecular mechanism of brain protection against convulsive brain damage in premature brains by observing the changes of apoptotic-regulating genes of bcl-2 and c-Jun expression in the hippocampus in Wistar rats with different ages after status convulsion（SC）.Methods SC was induced in infant Wistar rats（IRs） and adult Wistar rats（ARs） by intraperitoneal injection of lithium-pilocarpine.The rats were sacrificed at 3 hrs,6 hrs,12 hrs,1 day,3 days and 7 days after SC（n=8）.Bcl-2 and c-Jun protein and mRNA levels were measured using immunocytochemistry,RT-PCR and in situ hybridization.Results c-Jun protein levels increased significantly at 3 hrs and reached the peak at 6 hrs after SC in both IRs and ARs compared to those in the normal control group（P〈0.01）.c-Jun protein levels started to decrease 12 hrs after SC in both IRs and ARs.The expression of c-Jun protein in IRs returned to the basal level 1 day after SC,while remained higher in ARs than in the normal control group by 7 days after SC.The expression of c-Jun protein in ARs was much higher than that in IRs from 6 hrs to 7 days after SC（P〈0.05）.c-Jun mRNA level was in parallel with the protein level as mentioned in IRs and ARs after SC.There were no changes observed in both bcl-2 protein and bcl-2 mRNA levels after SC in IRs and ARs.Conclusions SC may induce an up-regulation of proapoptotic gene c-Jun in the hippocampus after SC,with a less strong extent and shorter duration in IRs compared to that in ARs.This might be one mechanism of brain protection against convulsive brain damage in IRs.The expression of bcl-2 remains unchanged after SC and is not affected by age in both IRs and ARs.