Long Non-Coding Rna Hulc Protects Against Atherosclerosis Via Inhibition Of Pi3k/Akt Signaling Pathway

Studies on the roles of long non-coding RNA in atherosclerosis (AS) have been extensively explored. However, the action of lncRNA highly upregulated in liver cancer (HULC) in AS still needs in-depth investigations. Hence, this study is launched towards the translation of HULC-oriented mechanism in AS. Mouse AS models were established by high cholesterol and high fat feeding. AS mice were injected with restored HULC or phosphatidylinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway inhibitor to explore their roles in AS. Blood lipid, inflammation and oxidative stress were detected as well as HULC, PI3K, phosphated-PI3K (p-PI3K), AKT, p-AKT, and aortic vascular cell apoptosis were determined. HULC was poorly expressed, p-PI3K and p-AKT were highly expressed in AS. HULC inhibited the PI3K/AKT signaling pathway. In AS, by inhibition of PI3K/AKT signaling pathway, restored HULC restrained atherosclerotic plaque formation, alleviated aortic intimal damage and reduced collagen fiber content in aorta, down-regulated blood lipid levels, and inhibited inflammation, oxidative stress and aortic vascular cell apoptosis. Our study elucidates that HULC alleviates AS via inhibition of the PI3K/AKT signaling pathway, which provides a potential biomarker for treatment of AS.