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

Abstract

Background. 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.Objectives. 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. Materials and methods.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.Results. 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.Conclusions. 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.

Progress in Research on the Mechanisms and Interventions of Phlebitis from the Perspective of Vascular Endothelial Cell and Signaling Pathway

“…Wang et al examined whether α-solanine had impacts on endothelial inflammation via the nuclear factor kappa B (NF-κB) signaling. 4 Human umbilical vein endothelial cells (HUVECs) overexpressing tumor necrosis factor alpha (TNF-α) were constructed. Compared to control cells, TNF-α-overexpressing cells showed significantly less viability and higher levels of TNF-α, interleukin 6 (IL-6), p-P65, p-IκBα, and IKKα/β.…”

Unraveling the therapeutic potential of ginsenoside compound Mc1 in Alzheimer’s disease: Exploring the role of AMPK/SIRT1/NF-κB signaling pathway and mitochondrial function

“…After preparing supernatants, an amount of about 30 µg of protein from each sample was separated with sodium dodecyl-sulfate polyacrylamide gel electrophoresis (SDS-PAGE) followed by an electrophoretic transfer to a nitrocellulose membrane (Bio-Rad, Hercules, USA). 30 The membrane was then placed in a dish containing 5% non-fat dry milk blocking buffer in Tris-buffered saline and 0.1% Tween 20 (TBST) for 1 h. This stage was followed by the incubation of the membranes with primary antibodies against total AMPK, phosphorylated AMPK, SIRT1, PGC-1α, phosphorylated p65-NFκB (1:1500; Cell Signaling Technology (CST), Danvers, USA), and GAPDH (1:1000; CST) in TBST at 4°C. After washing the membranes 5 times with TBST, they were soaked in HRP-conjugated secondary antibody (1:1500; SCT).…”