Introduction:
Carotid atherosclerosis (CAS) is one of the main causes of cerebral infarction in the ageing population. Long non-coding RNA small nucleolar RNA host gene 16 (lnc-SNHG16) could promote the development of atherosclerosis. However, the mechanism of lnc-SNHG16 in CAS remains vague.

Material and methods:
The expression levels of lnc-SNHG16, microRNA-30c-5p (miR-30c-5p) and disintegrin and metalloproteinase 10 (ADAM10) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and migration were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays, severally. The levels of interleukin-6 (IL-6), IL-β and tumor necrosis factor-α (TNF-α) were assessed by enzyme-linked immunosorbent assay (ELISA). Protein levels of spinal muscular atrophy (SMA), calponin and ADAM10 were examined by western blot assay. The binding relationship between miR-30c-5p and lnc-SNHG16 or ADAM10 was predicted by Starbase, then verified by the dual-luciferase reporter assay.

Results:
Lnc-SNHG16 and ADAM10 were increased, and miR-30c-5p was decreased in CAS patient and oxidized low-density lipoprotein (ox-LDL)-treated human aortic smooth muscle cells (hASMCs). Lnc-SNHG16 silencing repressed cell viability, migration, inflammation, facilitated differentiation in ox-LDL-treated hASMCs. Moreover, mechanical analysis proved that lnc-SNHG16 improved ADAM10 expression by sponging miR-30c-5p.

Conclusions:
Our data indicated that lnc-SNHG16 could regulate the progression of ox-LDL induced CAS model by the miR-30c-5p/ADAM10 axis, implying a potential therapeutic strategy for CAS