miRNA-323a-3p promoted intracranial, aneurysm-induced inflammation via AMPK/NF-κB signaling pathway by AdipoR1.

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.