Berberine Protects against TNF-α-Induced Injury of Human Umbilical Vein Endothelial Cells via the AMPK/NF-κB/YY1 Signaling Pathway.
Berberine Protects against TNF-α-Induced Injury of Human Umbilical Vein Endothelial Cells via the AMPK/NF-κB/YY1 Signaling Pathway.
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小檗碱通过 AMPK/NF-κB/YY1 信号通路防止 TNF-α 诱导的人脐静脉内皮细胞损伤
DOI：
10.1155/2021/6518355
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Shi DZ
中科院分区：
文献类型：
--
作者：
Chen L;Fan XD;Qu H;Bai RN;Shi DZ
内皮损伤是动脉粥样硬化(AS)的初始阶段，以炎症反应和通透性增加为特征。腺苷5‘-单磷酸、活化蛋白激酶和核因子-kappaB(NF-κB)/阴阳1(YY1)信号通路在血管内皮细胞损伤过程中发挥重要作用。黄连素(berberine，BBR)是从多种中草药中分离得到的生物活性生物碱，具有抗炎、抗菌、抗糖尿病、抗癌、抗氧化等多种药理作用。以往的研究表明，黄连素对血管内皮细胞损伤有保护作用。然而，潜在的机制仍不清楚。探讨补肾活血方对肿瘤坏死因子α诱导的人脐静脉内皮细胞损伤的潜在作用，并探讨其可能的分子机制。本研究将人脐静脉内皮细胞分为三组。细胞计数试剂盒-8法检测HUVEC活性。用乳酸脱氢酶漏出法测定细胞外乳酸脱氢酶(LDH)浓度。用流式细胞仪分析内皮细胞微粒子(EMP)数量。采用酶联免疫吸附试验(EL ISA)检测促炎细胞因子的表达。实时定量聚合酶链式反应(RT-κ)检测NF-YY1mRNA的表达。免疫荧光显微镜和免疫印迹法检测NF-κB、YY1和AMPK的蛋白表达。结果表明，在肿瘤坏死因子-β损伤的内皮细胞中，乳酸脱氢酶浓度、EMPs数和促炎细胞因子(IL-6、IL-8和IL-1α)的表达增加，但经补肾活血方处理后有所改善。补肾活血方可上调损伤内皮细胞磷酸化AMPK的表达，下调NF-κB和YY1的表达，并被AMPK抑制剂C(CC)所抵消。结果表明，BBR通过AMPK/NF-αB/YY1信号通路对肿瘤坏死因子-κ诱导的内皮损伤具有保护作用。
Endothelial injury, characterized by an inflammatory response and increased permeability, is an initial stage of atherosclerosis (AS). Adenosine 5′-monophosphate (AMP), activated protein kinase (AMPK), and Nuclear Factor kappa B (NF-κB)/Yin Yang 1(YY1) signaling pathways play important roles in the process of endothelial injury. Berberine (BBR), a bioactive alkaloid isolated from several herbal substances, possesses multiple pharmacological effects, including anti-inflammatory, antimicrobial, antidiabetic, anticancer, and antioxidant activities. Previous studies showed a protective effect of berberine against endothelial injury. However, the underlying mechanism remains unclear. We explored the potential effect of BBR on TNF- (tumor necrosis factor-) α-induced injury of human umbilical endothelial cells (HUVECs) and studied its possible molecular mechanism. In the present study, HUVECs were divided into three groups. HUVEC viability was measured with Cell Counting Kit-8 assay. Extracellular lactic dehydrogenase (LDH) concentration was measured with LDH leakage assay. Endothelial microparticle (EMP) numbers were evaluated by flow cytometry analysis assay. The expression of proinflammatory cytokines was evaluated by Enzyme-Linked Immunosorbent Assay (ELISA). The mRNA expression of NF-κB and YY1 was detected by Real-Time PCR (RT-PCR). The protein expression of NF-κB, YY1, and AMPK was detected by immunofluorescence microscopy assay or western blot analysis. The results showed that LDH concentration, EMPs numbers, and the expression of proinflammatory cytokines (IL-6, IL-8, and IL-1β) increased in TNF-α-induced injured HUVECs, but ameliorated by BBR pretreatment. BBR pretreatment upregulated the expression of phosphorylated AMPK and downregulated the expressions of NF-κB and YY1 in injured HUVECs induced by TNF-α, which were offset by the AMPK inhibitor Compound C (CC). The results indicated that BBR protected against TNF-α-induced endothelial injury via the AMPK/NF-κB/YY1 signaling pathway.
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10.1152/ajplung.00474.2006
发表时间：
2007-05-01
影响因子：
4.9
作者：
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影响因子：
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2012-09
期刊：
Arteriosclerosis, thrombosis, and vascular biology
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