在癫痫持续状态大鼠模型中，miR-210的下调通过负调控TLR4/NF-кB1信号通路促进海马神经元凋亡。
Downregulation of miR-210 Promoted Apoptosis of Hippocampal Neurons by Negatively Regulating the TLR4/NF-кB1 Signaling Pathway in a Rat Model of Status Epilepticus.
作者信息
Zhou Qin, Luo Huanjun, Wang Xiaowei, Li Peng, Kong Haibo, He Baomei
机构信息
Center for Reproductive Medicine, Department of Pediatrics, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, People's Republic of China.
Bengbu Medical College, Bengbu, Anhui Province, People's Republic of China.
出版信息
Neuropsychiatr Dis Treat. 2022 Aug 18;18:1763-1770. doi: 10.2147/NDT.S371950. eCollection 2022.
PURPOSE
Status epilepticus (SE) is a life-threatening condition causing brain damage, hippocampal necrosis and apoptosis. This study aimed to determine whether microRNA-210 regulates seizure and apoptosis by targeting the TLR4 /NF-κB1 associated signaling pathway.
METHODS
In a pilocarpine-induced epileptic rat model, the expressions of microRNA-210 (miR-210), TLR4, NF-κB1 and caspase-3 were assessed by a quantitative polymerase chain reaction and Western blotting. Tunel detects hippocampal neuron apoptosis.
RESULTS
We found that miR-210, TLR4, NF-κB1 and caspase-3 were upregulated in the hippocampus of the rat model compared with that of control. The knockdown of miR-210 significantly restored the expression levels of TLR4, NF-κB1 and caspase-3 and increased hippocampal apoptosis.
CONCLUSION
These findings showed that the downregulation of miR-210 promoted apoptosis of hippocampal neurons by negatively regulating the TLR4/NF-кB1 signaling pathway.
目的
癫痫持续状态（SE）是一种危及生命的疾病，可导致脑损伤、海马坏死和细胞凋亡。本研究旨在确定微小RNA-210是否通过靶向TLR4/NF-κB1相关信号通路来调节癫痫发作和细胞凋亡。
方法
在毛果芸香碱诱导的癫痫大鼠模型中，通过定量聚合酶链反应和蛋白质免疫印迹法评估微小RNA-210（miR-210）、TLR4、NF-κB1和半胱天冬酶-3的表达。Tunel检测海马神经元凋亡。
结果
我们发现，与对照组相比，大鼠模型海马中miR-210、TLR4、NF-κB1和半胱天冬酶-3上调。miR-210的敲低显著恢复了TLR4、NF-κB1和半胱天冬酶-3的表达水平，并增加了海马细胞凋亡。
结论
这些发现表明，miR-210的下调通过负调节TLR4/NF-κB1信号通路促进海马神经元凋亡。
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