ATHEROSCLEROSIS / RESEARCH PAPER
 
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Atherosclerosis has become a worldwide medical burden. Our previous studies have shown that Artemisinin(ART) had the capability to reduce atherosclerosis. Emerging evidence indicates that Long non-coding RNAs(lncRNAs) are engaged in the formation of atherosclerosis. However, whether lncRNAs might participate in the mechanism through which artemisinin mitigates atherosclerosis has not been reported.

Material and methods:
Eight-week-old apolipoprotein E deficient (APOE-/-) mice were divided into two groups, one of which was treated with Artemisinin. Red oil O staining was used to measure the sizes of Atherosclerotic lesion. We conducted deep sequencing to investigate lncRNA profiles in the aorta tissue in high-fat diet fed APOE knockdown mice with and without artemisinin treatment. CeRNA network, Kyoto Encyclopedia of Genes and Genomes(KEGG) and Gene Ontology(GO) analyses were constructed through bioinformatics analysis. RT-PCR was used to validate the differentially expressed lncRNAs.

Results:
A total of 102 lncRNAs and 4,630 mRNAs were differentially expressed (p<0.05) between the Artemisinin treatment group and atherosclerosis model group. KEGG and GO analyses indicated that the categories metabolic process, specific amino acid degradation and PI3K-Akt signaling pathway are involved in the effects of artemisinin treatment in atherosclerosis(qvalue<0.05). LncRNA ENSMUST00000099676.4, ENSMUST00000143673.1, ENSMUST00000070085.5 and ENSMUST00000224554 might be engaged in treatment mechanism through which Artemisinin alleviates Atherosclerosis.

Conclusions:
These findings indicated the possible mechanism and therapeutic role of lncRNAs in Artemisinin treatment of atherosclerosis and provided a theoretical basis for the future application of Artemisinin in patients with atherosclerosis.

eISSN:1896-9151
ISSN:1734-1922