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.

中文翻译：

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长链非编码 RNA HULC 通过抑制 PI3K/AKT 信号通路预防动脉粥样硬化

关于长链非编码 RNA 在动脉粥样硬化 (AS) 中的作用的研究已被广泛探索。然而，lncRNA在AS肝癌（HULC）中高度上调的作用仍需要深入研究。因此，本研究旨在将面向 HULC 的机制在 AS 中进行翻译。通过高胆固醇和高脂肪喂养建立小鼠AS模型。向 AS 小鼠注射恢复的 HULC 或磷脂酰肌醇 3-激酶/蛋白激酶 B (PI3K/AKT) 信号通路抑制剂，以探索它们在 AS 中的作用。检测血脂、炎症和氧化应激，并测定 HULC、PI3K、磷酸化 PI3K（p-PI3K）、AKT、p-AKT 和主动脉血管细胞凋亡。HULC 低表达，p-PI3K 和 p-AKT 在 AS 中高表达。HULC 抑制 PI3K/AKT 信号通路。在AS中，通过抑制 PI3K/AKT 信号通路，恢复 HULC 抑制动脉粥样硬化斑块的形成，减轻主动脉内膜损伤，减少主动脉中的胶原纤维含量，下调血脂水平，抑制炎症、氧化应激和主动脉血管细胞凋亡。我们的研究阐明了 HULC 通过抑制 PI3K/AKT 信号通路缓解 AS，这为治疗 AS 提供了潜在的生物标志物。