Furthermore, reducing Trim47 apparently decreased the release of pro-inflammatory factors, including interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS), in brain samples of MCAO rats, which was partly by the blockage of nuclear factor-kappa B (NF-κB) signaling.
Following middle cerebral artery occlusion/reperfusion (MCAO/R) surgery, rats were treated orally with 32, 16, and 8 mg/kg AR respectively for 14 days during which cerebral injury was evaluated and proinflammatory factors tumor necrosis factor-α and interleukin-6 as well as neurotrophic factors brain-derived neurotrophic factor and Neurotrophin-3 levels were determined with ELISA kits.
BV2 cells under OGD for 0, 6, 12, or 24 h exhibited decreased USP18 expression and increased expression of the proinflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, and interferon (INF)-γ. Lentiviral overexpression of USP18 in MCAO mice significantly decreased the infarct volume and significantly increased the number of new neurons that coexpressed bromodeoxyuridine (BrdU)/neuronal nuclei (NeuN).
In this work, male rats were treated with JNK-IN-8 after transient middle cerebral artery occlusion, and then the modified improved neurological function score (mNSS), the foot-fault test (FFT), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels were assessed.