MiR-181a influences the cognitive function of epileptic rats induced by pentylenetetrazol
MiR-181a influences the cognitive function of epileptic rats induced by pentylenetetrazol
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MiR-181a对戊四氮致癫痫大鼠认知功能的影响
DOI：
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发表时间：
2015
影响因子：
1.4
通讯作者：
Wu Yuan
中科院分区：
文献类型：
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作者：
Huang Yiqing;Liu Xixia;Liao Yuhan;Luo Chun;Zou Donghua;Wei Xing;Huang Qi;Wu Yuan
我们前期的研究表明，miR-181a在戊四氮（PTZ）致癫痫大鼠记忆障碍组中表达上调，但miR-181a是否影响PTZ致癫痫大鼠的认知功能仍不清楚。因此，我们研究了 miR-181a 在 PTZ 诱导的癫痫大鼠认知功能中的作用。通过 PTZ 点燃在 SD 雄性大鼠中诱导颞叶癫痫 (TLE) 模型。将癫痫大鼠分为癫痫组、Agomir对照组、miR-181a agomir组，每组12只。 12只大鼠作为假手术组。我们发现与假手术组相比，癫痫组中miR-181a的表达增加。我们还通过莫里斯水迷宫测试发现，第5天的逃避潜伏期延长，第6天的穿越次数减少，这可能表明记忆障碍。此外，miR-181a的过度表达有效降低了海马中Bcl-2蛋白水平并增加了细胞凋亡。此外，与Agomir对照组相比，miR-181a agomir组的逃避潜伏期明显诱导（P<0.05）。我们的研究结果表明，miR-181a可能在损害PTZ诱导的癫痫大鼠的认知功能中发挥作用，并且miR-181a可以降低Bcl-2蛋白并诱导海马细胞凋亡，这可能是损害认知功能的途径。
Our previous study showed that the expression of miR-181a in memory impairment group of pentylenetetrazol (PTZ)-induced epileptic rats was up-regulated, but whether miR-181a influenced the cognitive function of PTZ-induced epileptic rats remains unknown. Therefore, we investigated the role of miR-181a in the cognitive function of PTZ-induced epileptic rats. A model of temporal lobe epilepsy (TLE) was induced via PTZ kindling in SD male rats. The epileptic rats were divided into Epilepsy group, Agomir-control group, miR-181a agomir group, 12 rats for each. 12 rats were used as sham group. We found that compared to the sham group, the expression of miR-181a in the Epilepsy group was increased. We also found that escape latency in the 5th day was prolonged and crossing times in the 6th day was reduced via Morris Water Maze test, which may indicate memory impairment. Furthermore, over-expression of miR-181a effectively reduced Bcl-2 protein level and increased apoptosis in hippocampus. Moreover, compared with Agomir-control group, the escape latency of miR-181a agomir group was obviously induced (P<0.05). Our findings suggest that miR-181a may play a role in impairing the cognitive function of PTZ-induced epileptic rats, and miR-181a could decrease the Bcl-2 protein and induce the apoptosis in the hippocampus that might be the way to impair cognitive function.