Background: An intracranial arterial wall which locally protrudes outward, typically in the capsule and fusiform, is called an intracranial aneurysm (IA). Among these aneurysms, 1-2% might spontaneously rupture before treatment. Anterior and posterior communicating aneurysms are more likely to rupture than other aneurysms, and an anterior communicating aneurysm is more likely to rupture than a posterior communicating aneurysm.
Objectives: To identify the effects of miRNA-323a-3p expression in intracranial aneurysms and its potential regulatory mechanism.
Material and methods: Patients with IA and healthy volunteers were enrolled, and their serum samples were extracted for the detection of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), IL-6, IL-18, and miRNA-323a-3p. Then, the regulatory effects of miRNA-323a-3p on the above inflammatory factors and AdipoR1/AMPK/NF-kb signaling were also detected in vitro.
Results: The downregulation of miRNA-323a-3p reduced the expression of inflammatory factors (TNF-α, IL-1β, IL-6, and IL-18) in an in vitro model in comparison with the control group. The overexpression of miRNA-323a-3p suppressed the protein expression of adiponectin receptor R1 (AdipoR1) and p-AMPK, and induced NF-κB-p65 protein expression in an in vitro model.
Conclusions: We showed that AdipoR1 plasmid, AMPK activator 1 or si-NF-κB reduced the pro-inflammatory effects of miRNA-323a-3p in an in vitro model. The miRNA-323a-3p exacerbated the inflammatory reaction in IA through AMPK/NF-κB signaling by AdipoR1. Our findings suggest that miRNA-323a-3p targeting AdipoR1 is promising in further anti-inflammatory treatment of IAs.
Keywords: ADIPOR1; AMPK; NF-κB; intracranial aneurysm; miRNA-323a-3p.