Chen Zhang1, Deren Hou2, Xialu Feng2. 1. Department of Neurology, Third Xiangya Hospital, Central South University, Changsha, China zhangchen1208@hotmail.com. 2. Department of Neurology, Third Xiangya Hospital, Central South University, Changsha, China.
Abstract
BACKGROUND: The expression pattern and function of miRs in the post-status epilepticus (SE) rat are still unclear. This study aimed to investigate the role and mechanism of miR-181b in the post- SE rat. METHODS: The lithium-pilocarpine-induced SE model was established in Sprague-Dawley rats. The expression of miR-181b in rat blood and hippocampus was confirmed by RT-PCR at 24 hous and 7 days post-SE. The expression of Nrarp, Hes-1, and Bcl-2 was detected by RT-PCR and western blot. After the rat model was treated with LV-rno-mir181b and LV-anti-181b-5p, the expression change of miR-181b, Nrarp, Hes-1, and Bcl-2 was examined again. The effects of altering the expression of miR-181b on neurone cell apoptosis post-SE were assessed. RESULTS: The expression of miR-181b significantly decreased both in post-SE rat hippocampus and peripheral blood at 24 hours and 7 days (p<0.05). Nrarp is up-regulated, however, Hes-1 and Bcl-2 are down-regulated (p<0.05). LV-miR-181b treatment induced down-regulation of Nrarp and up-regulation of Hes-1 and Bcl-2 (p<0.05). Neurone cell apoptosis decreased in miR-181b group and post-SE rat hippocampal (p<0.05). CONCLUSIONS: Our study showed the low-expression of miR-181b in the hippocampus in a post-SE rat model. MiR-181b negatively regulated Nrarp as an anti-apoptotic gene via Notch signaling pathway.
BACKGROUND: The expression pattern and function of miRs in the post-status epilepticus (SE) rat are still unclear. This study aimed to investigate the role and mechanism of miR-181b in the post- SE rat. METHODS: The lithium-pilocarpine-induced SE model was established in Sprague-Dawley rats. The expression of miR-181b in rat blood and hippocampus was confirmed by RT-PCR at 24 hous and 7 days post-SE. The expression of Nrarp, Hes-1, and Bcl-2 was detected by RT-PCR and western blot. After the rat model was treated with LV-rno-mir181b and LV-anti-181b-5p, the expression change of miR-181b, Nrarp, Hes-1, and Bcl-2 was examined again. The effects of altering the expression of miR-181b on neurone cell apoptosis post-SE were assessed. RESULTS: The expression of miR-181b significantly decreased both in post-SE rat hippocampus and peripheral blood at 24 hours and 7 days (p<0.05). Nrarp is up-regulated, however, Hes-1 and Bcl-2 are down-regulated (p<0.05). LV-miR-181b treatment induced down-regulation of Nrarp and up-regulation of Hes-1 and Bcl-2 (p<0.05). Neurone cell apoptosis decreased in miR-181b group and post-SE rat hippocampal (p<0.05). CONCLUSIONS: Our study showed the low-expression of miR-181b in the hippocampus in a post-SE rat model. MiR-181b negatively regulated Nrarp as an anti-apoptotic gene via Notch signaling pathway.