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目的探讨新生大鼠反复惊厥前脑可塑性相关基因-1(PRG-1)的表达及生酮饮食(KD)对其表达的影响。方法日龄7d(P7)的SD大鼠24只。随机分为对照组(CON组)和惊厥组(RS组),每组各12只。适应性喂养1 d后,RS组大鼠吸入三氟乙醚诱导惊厥发作,反复诱导惊厥持续30 min,每日1次,同样方法连续诱导8 d;对照组同样操作,但不吸入三氟乙醚。在P21依据是否给予KD,每组大鼠再随机分为2组,即未惊厥普通饮食组(CON+ND)、未惊厥KD组(CON+KD)、惊厥普通饮食组(RS+ND)、惊厥KD组(RS+KD),每组各6只。CON+ND组和RS+ND组大鼠给予普通饮食,CON+KD组和RS+KD组大鼠给予KD,饮食干预3周。P42大鼠断头取大脑皮质及海马,用免疫印迹法检测各组大鼠脑组织皮质及海马PRG-1的表达。结果与CON+ND组比较,RS+ND组皮质及海马PRG-1表达均显著增高(Pa<0.05);与RS+ND组比较,RS+KD组皮质及海马PRG-1表达均明显降低(Pa<0.05);与CON+ND组比较,CON+KD组皮质及海马PRG-1的表达均无统计学差异(Pa>0.05)。结论新生大鼠反复惊厥远期PRG-1的表达增高,提示其参与发育期惊厥性脑损伤的病理生理机制。而KD可能通过下调惊厥组大鼠PRG-1表达,参与发育期惊厥性脑损伤的修复。
Objective To investigate the expression of PRG-1 in recurrent seizures and the effects of ketogenic diet (KD) on the expression of PRG-1 in neonatal rats. Methods 24 SD rats aged 7 days (P7). Randomly divided into control group (CON group) and convulsion group (RS group), each group of 12. After adaptive feeding for 1 d, rats in RS group were induced to seizure by inhalation of trifluoroethyl ether, convulsions were induced repeatedly for 30 min and once daily. The rats in RS group were induced for 8 d continuously. At P21, rats in each group were randomly divided into 2 groups: CON + ND group, CON + KD group, RS + ND group, Convulsive KD group (RS + KD), each group of 6. Rats in CON + ND group and RS + ND group were given normal diet. Rats in CON + KD group and RS + KD group were given KD for three weeks. The cerebral cortex and hippocampus of P42 rats were decapitated. The expression of PRG-1 in cerebral cortex and hippocampus was detected by Western blotting. Results Compared with CON + ND group, the expression of PRG-1 in cortex and hippocampus of RS + ND group was significantly increased (P <0.05). Compared with RS + ND group, the expression of PRG-1 in cortex and hippocampus of RS + Pa> 0.05). Compared with CON + ND group, the expression of PRG-1 in cortex and hippocampus in CON + KD group was not significantly different (P> 0.05). Conclusions The expression of PRG-1 in neonatal rats with recurrent seizures is increased, suggesting its involvement in the pathophysiologic mechanism of developing convulsive brain injury. However, KD may be involved in the repair of convulsive brain injury in developmental stage by downregulating the expression of PRG-1 in seizure rats.