He Rui, Tang Guo-Lin, Niu Lei, Ge Chang, Zhang Xiao-Qi, Ji Xiao-Feng, Fang Huang, Luo Zheng-Liang, Chen Min, Shang Xi-Fu
Department of Orthopedics, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China.
Ann Palliat Med. 2020 Mar;9(2):190-198. doi: 10.21037/apm.2020.02.13. Epub 2020 Mar 11.
In this study, we analyzed whether the neuroprotection of Circ 0000962 promoted neural inflammation in spinal cord injury (SCI) and its possible mechanism.
Inflammation factors (TNF-α, IL-1β, IL-6 and IL-18) were measured using ELIS kit, and NF-κB, PI3K and phosphorylation-(p)-Akt protein expression were analyzed by Western blot analysis.
Circ 0000962 expression was decreased in SCI model rat and vitro model. Over-expression of Circ 0000962 decreased inflammation in vitro model of SCI via activation of PI3K/Akt and suppression of NF-κB by down-regulation of miR-302b-3p. Down-regulation of Circ 0000962 promotion inflammation, suppressed NF-κB protein expression, and induced PI3K and p-Akt protein expression in vitro model of SCI by up-regulation of miR-302b-3p. MiR-302b-3p reduced the effect of Circ 0000962 on inflammation in vitro model.
This study showed that Circ 0000962 promoted nerve cell inflammation through Akt/ NF-κB signaling by PI3K in SCI.
在本研究中，我们分析了Circ 0000962的神经保护作用是否会促进脊髓损伤（SCI）中的神经炎症及其可能机制。
使用ELISA试剂盒检测炎症因子（TNF-α、IL-1β、IL-6和IL-18），并通过蛋白质印迹分析来分析NF-κB、PI3K和磷酸化（p）-Akt蛋白的表达。
在SCI模型大鼠和体外模型中，Circ 0000962的表达降低。Circ 0000962的过表达通过激活PI3K/Akt并下调miR-302b-3p来抑制NF-κB，从而减轻SCI体外模型中的炎症。在SCI体外模型中，Circ 0000962的下调通过上调miR-302b-3p促进炎症，抑制NF-κB蛋白表达，并诱导PI3K和p-Akt蛋白表达。MiR-302b-3p降低了Circ 0000962在体外模型中对炎症的影响。
本研究表明，在SCI中，Circ 0000962通过PI3K的Akt/NF-κB信号传导促进神经细胞炎症。
