Annals of Palliative Medicine · 2020 · 21 citations · 19 references
Life SciencesNeurobiologyNeuroscienceInflammationMolecular NeuroscienceNeuroimmunologyInflammatory Cell SignalingInflammatory SignalingNeuroinflammationNeuroprotectionSpinal Cord InjurySpinal Cord PathologyMicrorna In InflammationNerve Injury - Induced InflammationNeuroprotection In Spinal TraumaNf-κb SignalingPhosphoinositide 3-Kinase-akt SignalingSpinal Cord Injury NeuroprotectionSpinal Cord Injury PathologySpinal Cord Injury Pathophysiology
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.
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Ming-liang Ji, Jun Lü, Peiliang Shi et al. · Journal of Bone and Mineral Research · 2015 · 86 citations