Abstract：
Spinal cord injury (SCI) is a common disease of the central nervous system. circRNAs play a crucial role in neurological disease. The purpose of this study was to investigate the role of circ-KATNAL1 in SCI and its regulatory mechanism. T9-L10 spinal segment of Sprague Dawley rats was compressed or contused after T10 laminectomy to establish the SCI rat model. Then, rats were divided into SCI group, si-NC group, si-circ-KATNAL1 group, si-circ-KATNAL1 + antagomir NC group, si-circ-KATNAL1 + miR-98-5p antagomir group, si-circ-KATNAL1 + oe-NC group, and si-circ-KATNAL1 + oe-PRDM5 group, with 6 rats in each group. There was another sham operation group that received no treatment. Basso, Beattie, and Bresnahan (BBB) scores were used to evaluate the neural function of rats. In addition to that, the pathological changes of spinal cord tissue, neuronal apoptosis, and inflammatory responses were correspondingly observed and analyzed. Quantitative measurements of circ-KATNAL1, miR-98-5p, and PRDM5 levels were conducted, as well as analyses of their interrelationship. Circ-KATNAL1 was up-regulated in the spinal cord tissue of SCI rats, and circ-KATNAL1 knockdown could improve neural function, alleviate pathological changes of spinal cord tissue, and inhibit neuronal apoptosis and inflammatory responses in SCI rats. For miR-98-5p, circ-KATNAL1 was an upstream factor, while PRDM5 was a downstream actor. miR-98-5p deficiency or PRDM5 restoration impaired the remission effect of circ-KATNAL1 knockdown on SCI. Circ-KATNAL1 knockdown reduces neuronal apoptosis and alleviates SCI through miR-98-5p/PRDM5 regulatory axis.
摘要：
脊髓损伤（SCI）是中枢神经系统的常见疾病。circRNAs在神经系统疾病中起着至关重要的作用。目的探讨circ-KATNAL1在SCI中的作用及其调控机制。T10椎板切除术后，对SpragueDawley大鼠的T9-L10脊髓节段进行压迫或挫伤，建立SCI大鼠模型。然后，大鼠分为SCI组,si-NC组,si-circ-KATNAL1组，si-circ-KATNAL1+antagomirNC组，si-circ-KATNAL1+miR-98-5pantagomir组，si-circ-KATNAL1+oe-NC组，和si-circ-KATNAL1+oe-PRDM5组，每组6只大鼠。另一个假手术组没有接受治疗。巴索,Beattie,并采用BBB评分评价大鼠神经功能。除此之外,脊髓组织的病理变化，神经元凋亡，和炎症反应进行了相应的观察和分析。circ-KATNAL1，miR-98-5p，进行了PRDM5水平测定，以及对它们相互关系的分析。Circ-KATNAL1在SCI大鼠脊髓组织中表达上调,circ-katnal1基因敲除可以改善神经功能，减轻脊髓组织的病理变化，并抑制SCI大鼠神经元凋亡和炎症反应。对于miR-98-5p，Circ-KATNAL1是上游因素，而PRDM5是下游演员。miR-98-5p缺乏或PRDM5恢复损害了circ-KATNAL1敲低对SCI的缓解作用。Circ-KATNAL1敲低通过miR-98-5p/PRDM5调节轴减少神经元凋亡并减轻SCI。
