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Alpha-solanine inhibits endothelial inflammation via nuclear factor kappa B signaling pathway

肿瘤坏死因子α 免疫印迹 活力测定 脐静脉 分子生物学 转染 信号转导 化学 炎症 IκB激酶 内皮干细胞 NF-κB 人脐静脉内皮细胞 细胞 生物 体外 免疫学 生物化学 基因
作者
Nan Wang,Da-Quan Jiang,Chunxiu Zhou,Xi Han
出处
期刊:Advances in Clinical and Experimental Medicine [Wroclaw Medical University]
卷期号:32 (8): 909-920 被引量:5
标识
DOI:10.17219/acem/158781
摘要

Alpha-solanine (α-solanine) is the main glycoalkaloid in potato plants. It possesses anticarcinogenic properties and exerts toxic effects. Alpha-solanine can regulate the nuclear factor kappa B (NF-κB) signaling pathway in cancer cells and macrophages. However, little is known about the anti-inflammatory effects and the related molecular mechanisms of α-solanine on endothelial cells.This study aims to examine the effects of α-solanine on endothelial inflammation in vitro, and to evaluate its influence on regulating the NF-κB signaling pathway.Tumor necrosis factor alpha (TNF-α)-pcDNA3.1(+) plasmid vector was constructed and transfected into human umbilical vein endothelial cells (HUVECs). The expression of TNF-α was examined with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot. Following treatment with α-solanine or the specific NF-κB inhibitor SN50 for 24 h, cell viability was detected using Cell Counting Kit-8 (CCK-8) assay. Interleukin 6 (IL-6) and TNF-α levels in cell supernatant were detected using enzyme-linked immunosorbent assay (ELISA). The relative protein levels of phospho-P65 (p-P65), phospho-inhibitor of NF-κBα (p-IκBα) and IκB kinase (IKK) α/β were examined with western blot.The α-solanine inhibits TNF-α-induced inflammatory injury in HUVECs. Compared with control cells, the cell viability was significantly decreased, the levels of TNF-α and IL-6 were significantly increased, and the relative protein levels of p-P65, p-IκBα and IKKα/β were significantly upregulated in TNF-α-overexpressed cells. The treatment with α-solanine or SN50 decreased the levels of TNF-α and IL-6, and downregulated the relative protein levels of p-P65, p-IκBα and IKKα/β in TNF-α-overexpressed HUVECs.This study demonstrated for the first time that α-solanine inhibits endothelial inflammation through the NF-κB signaling pathway. The α-solanine was suggested to be an inhibitor of the NF-κB signaling pathway in endothelial cells. The anti-inflammatory effect of α-solanine may provide a new perspective for the prevention and treatment of phlebitis.

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