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当归有机酸对 ox-LDL 诱导的 HUVECs 自噬功能障碍的保护作用。

The protective effects of angelica organic acid against ox-LDL-induced autophagy dysfunction of HUVECs.

机构信息

School of Basic Medical Sciences, Lanzhou University, Lanzhou, 730000, China.

Gansu Provincial Hospital, Lanzhou, 730000, China.

出版信息

BMC Complement Med Ther. 2020 Jun 1;20(1):164. doi: 10.1186/s12906-020-02968-7.

Abstract

BACKGROUND

Angelica root is the dry root of the Umbelliferae plant Angelica sinensis (oliv) Diels. Angelica organic acid (OA) is the main active ingredient in Angelica sinensis, and it exerts potential anti-atherosclerotic effects by preventing Oxidized low-density lipoprotein (Ox-LDL) induced endothelial injury. To study the protective effects of OA on ox-LDL-induced HUVECs autophagic flux dysfunction and inflammatory injury.

METHODS

OA were isolated by water extraction and alcohol precipitation, and then the content of ferulic acid (FA) in the OA was determined by high performance liquid chromatography. The ox-LDL-induced endothelial injury model was established. The effect of ferulic acid on the survival of Human umbilical vein endothelial cells (HVUECs) was detected by CCK-8 assay. HUVECs were pretreated with different concentrations of OA (20 μmol/L, 40 μmol/L, and 80 μmol/L), and Western Blot was used to detect the expressions of LC3II, p62, MCP-1, VCAM-1 and LOX-1. The autophagosomes in HUVECs were observed by transmission electron microscopy (TEM).

RESULTS

20 μmol/L OA could increase the expression of LC3II and decrease the expression of p62, MCP-1, VCAM-1 and LOX-1. The results of TEM showed that angelica organic acids promoted cell organelle degradation in autolysosomes.

CONCLUSION

OA could reduce inflammation, protect endothelial cells and play an anti-atherosclerotic role by enhancing the autophagy flux of damaged endothelial cells, in which FA the major active ingredient of OA played a major role.

摘要

背景

当归根是伞形科植物当归(Oliv)Diels 的干燥根。当归有机酸(OA)是当归的主要活性成分,通过防止氧化型低密度脂蛋白(Ox-LDL)诱导的内皮损伤,发挥潜在的抗动脉粥样硬化作用。本研究旨在探讨 OA 对 Ox-LDL 诱导的 HUVEC 自噬流功能障碍和炎症损伤的保护作用。

方法

采用水提醇沉法提取 OA,采用高效液相色谱法测定 OA 中阿魏酸(FA)的含量。建立 Ox-LDL 诱导的内皮损伤模型。采用 CCK-8 法检测 FA 对人脐静脉内皮细胞(HUVEC)活力的影响。用不同浓度的 OA(20μmol/L、40μmol/L、80μmol/L)预处理 HUVECs,Western blot 检测 LC3II、p62、MCP-1、VCAM-1 和 LOX-1 的表达。透射电镜(TEM)观察 HUVEC 中的自噬体。

结果

20μmol/L OA 可增加 LC3II 的表达,降低 p62、MCP-1、VCAM-1 和 LOX-1 的表达。TEM 结果表明,当归有机酸促进了自噬溶酶体中细胞细胞器的降解。

结论

OA 通过增强受损内皮细胞的自噬流来减少炎症、保护内皮细胞并发挥抗动脉粥样硬化作用,其中 FA 是 OA 的主要活性成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e9d/7268640/b94b7d998ff9/12906_2020_2968_Fig1_HTML.jpg

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