Background: In this study, we analyzed whether the neuroprotection of Circ 0000962 promoted neural inflammation in spinal cord injury (SCI) and its possible mechanism.
Methods: 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.
Results: 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.
Conclusions: This study showed that Circ 0000962 promoted nerve cell inflammation through Akt/ NF-κB signaling by PI3K in SCI.
Keywords: Akt; Circ 0000962; NF-κB; PI3K; inflammation; miR-302b-3p; neural apoptosis; spinal cord injury (SCI).