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

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

  • Cell Cycle. 2020 Jun;19(11):1253-1264. doi: 10.1080/15384101.2020.1731652.
Yingying Zhang 1 Binghui Hou 1 Chunxiao Li 1 Hong Li 1


  • 1 Department of Neurology, The Affiliated Hospital of Qingdao University , Qingdao, 266000, Shandong, China.

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.


Encephalitis; TNF-α; circARF3; inflammation; miR-125b.