【摘要】 目的 探讨高良姜素（Gal）对内皮炎症和动脉粥样硬化（AS）发生发展的拮抗作用及可能的作用机制。方法 将APOE^-/-小鼠随机分为溶媒组和Gal组。喂食12周高脂饲料，在第8周Gal组灌胃80 mg/（kg·d）的Gal进行干预，检测低密度脂蛋白、总胆固醇、三酰甘油、高密度脂蛋白的水平，油红O染色法检测斑块面积，qPCR法检测主动脉弓以及其内膜处ICAM1、CD62e的mRNA表达。人脐静脉内皮细胞（HUVEC）中加入肿瘤坏死因子-α（TNF-α）、Gal、STAT3激动剂（Colivelin）处理，CCK8实验检测细胞活力，qPCR法和Western blot检测ICAM1、VCAM1、CD62e的mRNA和蛋白表达以及p-STAT3、p-JAK2的蛋白表达，内皮细胞黏附试验检测THP-1细胞黏附于HUVECs相对密度。结果 与溶媒组相比，Gal显著减少小鼠主动脉大体及其根部粥样斑块形成，减低小鼠血浆中低密度脂蛋白、总胆固醇和三酰甘油水平，升高高密度脂蛋白水平；Gal使小鼠主动脉弓部及其内膜的ICAM1和CD62e的mRNA表达减低。50μmol·L^-1 Gal对HUVECs无毒性；TNF-α均可使HUVECs中ICAM1、CD62e、VCAM1的mRNA和蛋白表达以及p-STAT3、p-JAK2蛋白表达升高；TNF-α可使黏附于HUVECs的THP-1细胞个数增加。Gal加入后可显著降低ICAM1、CD62e、VCAM1的mRNA和蛋白表达以及p-STAT3、p-JAK2蛋白表达；Gal使得黏附于HUVECs的THP-1细胞个数减少。与TNF-α+Gal组相比，Colivelin增加ICAM1和VCAM1的蛋白表达。结论 Gal通过抑制JAK2-STAT3磷酸化减轻小鼠内皮炎症改善动脉粥样硬化。更多还原

【Abstract】 Objective To determine the inhibition of galangin（Gal） on the endothelial inflammation and atherosclerosis（AS） formation and related mechanism. Methods APOE^-/- mice were randomly divided into a vehicle group and a Gal group. High-fat diet was fed for 12 weeks. The mice in the Gal group were treated with 80 mg/（kg·d） Gal by gavage from the 8th week. The levels of LDL-C, total cholesterol, triglycerides and HDL-C were detected. The area of plaque was detected by oil Red O staining. The mRNA expressions of ICAM1 and CD62e were detected by qPCR in the aortic arch and its intima. Human umbilical vein endothelial cells（HUVECs） were treated with tumor necrosis factor-α（TNF-α）, Gal and STAT3 agonist（Colivelin）. The cell viability was detected by CCK8 assay. The mRNA and protein expressions of ICAM1, VCAM1 and CD62e as well as the protein expressions of p-STAT3and p-JAK2 were detected by qPCR and Western blot. The relative density of THP-1 cells adhering to HUVECs was detected by the endothelial cell adhesion test. Results Compared with the vehicle group,Gal significantly reduced the formation of atherosclerotic plaque in the aorta and its root, decreased the levels of low-density lipoprotein, total cholesterol and triglyceride, and increased the level of highdensity lipoprotein in the plasma of mice. Gal at 50 μmol·L^-1 showed no toxicity to HUVECs. The m RNA expression of ICAM1 and CD62e was decreased in the aortic arch and its intima of mice. The m RNA and protein expression of ICAM1, CD62e, VCAM1 and the protein expression of p-STAT3 and p-JAK2 in HUVCEs were significantly increased in the TNF-α groups. TNF-α increased the number of THP-1 monocytes adhering to HUVECs. After adding Gal, The mRNA and protein expression of ICAM1, CD62e and VCAM1 as well as the protein expression of p-STAT3 and p-JAK2 was significantly increased. Compared with the TNF-α + Gal group, the protein expression of ICAM1 and VCAM1 was increased by colivelin. Conclusion Galangin may alleviate the endothelial inflammation and attenuate the atherosclerosis via inhibiting JAK2-STAT3 phosphorylation in mice.更多还原