中文摘要：

目的探讨香芹酚对癫癇持续状态大鼠海马损伤、神经细胞凋亡及内质网应激相关因子GRP78、caspase12、CHOP表达的影响。方法成年雄性SD大鼠80只,随机分为正常对照组、模型对照组、香芹酚小剂量（30 mg·kg^-1）组及香芹酚大剂量（60 mg·kg^-1）组,每组20只。建立氯化锂-匹罗卡品大鼠癫癇持续状态模型,采用Nissl及TUNEL染色法检测海马损伤、神经细胞凋亡,采用Western blot法检测海马内质网应激相关因子的表达变化。结果正常对照组、模型对照组、香芹酚小剂量组及香芹酚大剂量组神经细胞凋亡指数分别为（5.08±3.00）,（34.43±0.55）,（15.28±3.97）,（10.62±2.56）;香芹酚小、大剂量组均较模型对照组GRP78升高（P〈0.01）,caspase12和CHOP表达降低（P〈0.01）,且香芹酚大剂量组改善更明显。结论香芹酚对癫癇大鼠海马神经具有明显的保护作用,且与剂量呈正相关,其机制可能是增加GRP78表达以应对损伤,降低caspase12及CHOP的表达以抑制内质网应激引起的凋亡。

英文摘要：

Objective To investigate the effect of carvacrol on hippocampal injury,neurocyte apoptosis and endoplasmic reticulum stress related molecules like GRP78,caspase12,and CHOP in epileptic rats. Methods The total of 80 male SD rats were randomly divided into normal control,model control,carvacrol at low dose（ 30 mg · kg^-1） and high dose（ 60 mg·kg^-1） groups,20 rats in each group. The consistent epilepticus model was established by treating lithium chloridepilocarpine in rats.The neuronal injury and apoptosis were detected by Nissl staining and TUNEL staining,respectively.The levels of GRP78,caspase12 and CHOP were measured by Western blot analysis. Results The nerve cell apoptosis index of the normal controls,model controls,carvacrol at low dose and that at high dose were（ 5.08± 3.00）,（ 34.43± 0.55）,（ 15.28± 3.97）,（ 10.62±2.56）,respectively. Compared with the model control,carvacrol pretreatment significantly attenuated the hippocampal injury,increased the expression of GRP78 and decreased the expression of caspase12 and CHOP,especially for carvacrol at high dose. Conclusion Carvacrol plays a role in hippocampus injury protection,which is in a dose-dependent manner and involved inpromoting GRP78 against hippocampal injury,mitigating caspase12 and CHOP induced ER apoptosis in epileptic rat.