红藻氨酸诱导癫痫大鼠前脑CX32的表达及辛醇干预的影响

The expression of connexin32 within the procerebrum of the epilepsy rats induced with Kainic acid and interventional influence of octanol

目的观察红藻氨酸(kainic acid,KA)诱导癫痫大鼠前脑缝隙连接蛋白32(connexin 32,CX32)的表达及辛醇干预的影响。方法用免疫荧光法检测癫痫发作后各时间点大鼠皮质及海马CX32阳性细胞表达。同时观察致痫前给予辛醇干预对大鼠皮质及海马CX32阳性细胞表达的影响。结果 KA致痫组大鼠皮层及海马CX32阳性细胞在各时程明显高于正常对照组(P<0.05),并且随时程延长呈增加趋势,7d达高峰,在海马中的变化比皮层明显,但无统计学意义(P>0.05)。辛醇干预组大鼠皮层及海马CX32阳性细胞在各相应时程明显低于KA致痫组(P<0.01)。结论 CX32组成缝隙连接(gap junction,GJ)在癫痫的发生发展过程中起重要作用,辛醇可以减少癫痫大鼠CX32表达,降低癫痫敏感性,实现脑保护作用。

Objective To observe the expression of connexin32 within the procerebrum of the epilepsy rats induced with Kainic acid and interventional influence of octanol.Methods The expression of CX32 positive cells at different time points in cortex and hippocampus of the epilepsy rats induced with Kainic acid was detected by immumoflourescence method.Meanwhile,the effects of octanol intervention on the expression of CX32 positive cells in cortex and hippocampus of rat brain administered before epilepsy was evaluated.Results The expression of CX32 positive cells in cortex and hippocampus in the group of epilepsy-rats induced by kainic acid was higher than that in normal control group at different time points（P0.05）,and increased gradually,reached peak on 7d.The change in hippocampus was more obvious than in cortex.However,there was no significant difference（P0.05）.The expression of CX32 positive cells in cortex and hippocampus in the group intervened by octanol was lower than that in the group of epilepsy-rats induced by kainic acid at corresponding time points（P0.01）.Conclusions The results indicate that gap junction via CX32 may play an important role in the occurrence and development of epilepsy.Octanol could reduce the expression of CX32 in procerebrum of the epilepsy rats,decrease susceptibility of epilepsy and implement protection of brain.