The recovery of spinal cord injury (SCI) involves multiple factors, of which miRNAs take an important part. In this study, we evaluated the function of microRNA-211−5p (miR-211−5p) on SCI in a rat model. SCI model was established using modified Allen's weight-drop method and Basso-Bcattie-Bresnahan score was applied to assess the locomotor function. MiR-211−5p agomir was utilized to increase miR-211−5p expression and endoplasmic reticulum (ER) stress inhibitor, 4-PBA (4-phenylbutyric acid), was utilized to suppress ER stress. Neuron apoptosis and the expressions of miR-211−5p, activating transcription factor 6 (ATF6), apoptosis-related proteins, pro-inflammatory cytokines and endoplasmic reticulum stress-related proteins were detected. Dual luciferase reporter gene assay was performed to verify the binding between miR-211−5p and ATF6. The results showed that miR-211−5p directly targeted ATF6. MiR-211−5p was down-regulated and ATF6 was up-regulated in SCI rats. Both interferences with miR-211−5p agomir and 4-PBA effectively attenuated neuron apoptosis and reversed the expressions of apoptosis, inflammation and endoplasmic reticulum stress-related molecules post SCI in rats. These findings demonstrated that miR-211−5p could effectively alleviate SCI-induced neuron apoptosis and inflammation via directly targeting ATF-6 and regulating ER stress.

脊髓损伤（SCI）的恢复涉及多种因素，其中miRNAs起着重要的作用。在这项研究中，我们在大鼠模型中评估了 microRNA-211-5p (miR-211-5p) 对 SCI 的功能。采用改良Allen's减重法建立SCI模型，并应用Basso-Bcattie-Bresnahan评分评估运动功能。MiR-211-5p agomir 用于增加 miR-211-5p 表达，内质网 (ER) 应激抑制剂 4-PBA（4-苯基丁酸）用于抑制 ER 应激。检测神经元凋亡和miR-211-5p、激活转录因子6（ATF6）、凋亡相关蛋白、促炎细胞因子和内质网应激相关蛋白的表达。进行双荧光素酶报告基因检测以验证 miR-211-5p 和 ATF6 之间的结合。结果表明 miR-211-5p 直接靶向 ATF6。MiR-211-5p 在 SCI 大鼠中下调，ATF6 上调。对 miR-211-5p agomir 和 4-PBA 的干扰都有效地减弱了神经元凋亡，并逆转了大鼠 SCI 后细胞凋亡、炎症和内质网应激相关分子的表达。这些发现表明 miR-211-5p 可以通过直接靶向 ATF-6 和调节内质网应激来有效缓解 SCI 诱导的神经元凋亡和炎症。