• Rui He, Guo-Lin Tang, Lei Niu, Chang Ge, Xiao-Qi Zhang, Xiao-Feng Ji, Huang Fang, Zheng-Liang Luo, Min Chen, and Xi-Fu Shang.
• 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 1; 9 (2): 190-198.

BackgroundIn this study, we analyzed whether the neuroprotection of Circ 0000962 promoted neural inflammation in spinal cord injury (SCI) and its possible mechanism.MethodsInflammation 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.ResultsCirc 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.ConclusionsThis study showed that Circ 0000962 promoted nerve cell inflammation through Akt/ NF-κB signaling by PI3K in SCI.

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