Overexpression of circARF3 mitigates TNF-α-induced inflammatory damage by up-regulating miR-125b.

Encephalitis is the highest disability illness. We studied the function and mechanisms of circular RNA circARF3 (circARF3) in neurocyte cell inflammatory damage. CCK-8 assay and flow cytometry were, respectively, employed for examining the influences of tumor necrosis factor α (TNF-α), circARF3 and microRNA (miR)-125b on cell viability and apoptosis. The expression of circARF3 and miR-125b were changed by employing cell transfection and the results were determined by using qRT-PCR. Besides, the expression of Bcl-2, Bax, Cleaved-caspase-3, interleukin (IL)-1β, IL-6, IL-8 and cell pathways-related proteins were examined by using Western blot. The productions of IL-6, IL-8 and IL-1β were also tested by ELISA. The level of reactive oxygen species (ROS) was examined by ROS assay. We found that TNF-α caused inflammatory damage showing as suppressed cell viability, enhanced cell apoptosis, and increased cytokines production and ROS generation. Besides, TNF-α inducement also markedly reduced circARF3 expression. circARF3 overexpression mitigated TNF-α-induced cell inflammatory damage. Moreover, miR-125b was targeted and positively regulated by circARF3. Furthermore, miR-125b inhibition could reverse the influences of circARF3 overexpression. Besides, circARF3 restrained the JNK and NF-κB pathways by up-regulation of miR-125b. In conclusion, overexpression of circARF3 mitigated cell inflammatory damage via inactivation of JNK and NF-κB pathways and thereby up-regulation of miR-125b.