Valproate (VPA) is capable of attenuating ischemic stroke (IS)-related disorders in brain tissues. Long non-coding RNAs (lncRNAs) are involved in the progression of IS. In the current study, the role of lncRNA RMRP in the protective effects of VPA against IS was explored. Mice were subjected to middle cerebral artery occlusion (MCAO) model to induce IS injures and then were administrated with VPA. The effects of VPA on infarction area and apoptosis in brain tissues, and the RMRP-regulated PI3K/Akt signaling activity were detected. Thereafter, oxygen-glucose deprivation (OGD) BV-2 cells were used as the in vitro model to further explore the mechanism underlying VPA function. The administration of VPA reduced infarction area and suppressed apoptosis in brain tissues of MCAO mice. VPA also inhibited RMRP expression and activated PI3K/Akt signaling. In OGD BV-2 cells, the treatment of VPA increased viability and attenuated apoptosis, which was associated with the inhibition of RMRP and the activation of PI3K/Akt pathway. Moreover, the induced expression of RMRP blocked the anti-OGD function of VPA, indicating the key role of RMRP inhibition in the effects of VPA on nerve system. Collectively, VPA attenuated MCAO/OGD-induced disorders in mice and microglia. The effects were dependent on the inhibition of RMRP, which subsequently induced the activation of PI3K/Akt signaling.

丙戊酸盐 (VPA) 能够减轻脑组织中与缺血性中风 (IS) 相关的疾病。长链非编码 RNA (lncRNA) 参与 IS 的进展。在目前的研究中，探讨了 lncRNA RMRP 在 VPA 对 IS 的保护作用中的作用。对小鼠进行大脑中动脉闭塞（MCAO）模型以诱导 IS 损伤，然后给予 VPA。检测VPA对脑组织梗死面积和细胞凋亡的影响，以及RMRP调节的PI3K/Akt信号活性。此后，氧葡萄糖剥夺（OGD）BV-2细胞被用作体外模型以进一步探索 VPA 功能的潜在机制。VPA的给药减少了MCAO小鼠脑组织的梗死面积并抑制了细胞凋亡。VPA 还抑制 RMRP 表达并激活 PI3K/Akt 信号。在OGD BV-2细胞中，VPA处理增加了细胞活力并减弱了细胞凋亡，这与RMRP的抑制和PI3K/Akt通路的激活有关。此外，RMRP的诱导表达阻断了VPA的抗OGD功能，表明RMRP抑制在VPA对神经系统的影响中起关键作用。总的来说，VPA 减轻了小鼠和小胶质细胞中 MCAO/OGD 诱导的疾病。这些效果取决于对 RMRP 的抑制，后者随后诱导了 PI3K/Akt 信号传导的激活。