Biochanin A inhibits lipopolysaccharide-induced inflammation in human umbilical vein endothelial cells

Ming, Xiaodong; Ding, Mingfeng; Zhai, Bo; Xiao, Lei; Piao, Taikui; Liu, Ming

doi:10.1016/j.lfs.2015.06.015

Cited by 50 publications

(28 citation statements)

References 38 publications

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“…). The inflammatory potential of PA and LPS to human endothelial cells is generally in agreement with previous reports (Cao et al ., ; Lu et al ., ; Ming et al ., ; Wu et al ., ). With the presence of PA or LPS, the release of inflammatory mediators or THP‐1 monocyte adhesion was not enhanced further by the exposure to NM110.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity, oxidative stress and inflammation induced by ZnO nanoparticles in endothelial cells: interaction with palmitate or lipopolysaccharide

Gong

Liu

et al. 2016

J. Appl. Toxicol.

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Recent studies showed that ZnO nanoparticles (NPs) might induce the toxicity to human endothelial cells. However, little is known about the interaction between ZnO NPs and circulatory components, which is likely to occur when NPs enter the blood. In this study, we evaluated ZnO NP-induced cytotoxicity, oxidative stress and inflammation in human umbilical vein endothelial cells (HUVECs), with the emphasis on the interaction with palmitate (PA) or lipopolysaccharide (LPS), because PA and LPS are normal components in human blood that increase in metabolic diseases. Overall, ZnO NPs induced cytotoxicity and intracellular reactive oxygen species (ROS) at a concentration of 32 μg ml , but did not significantly affect the release of inflammatory cytokines or adhesion of THP-1 monocytes to HUVECs. In addition, exposure to ZnO NPs dose-dependently promoted intracellular Zn ions in HUVECs. PA and LPS have different effects. Two hundred μm PA significantly induced cytotoxicity and THP-1 monocyte adhesion, but did not affect ROS or release of inflammatory cytokines. In contrast, 1 μg ml LPS significantly induced ROS, release of inflammatory cytokines and THP-1 monocyte adhesion, but not cytotoxicity. The presence of ZnO NPs did not significantly affect the toxicity induced by PA or LPS. In addition, the accumulation of Zn ions after ZnO NP exposure was not significantly affected by the presence of PA or LPS. We concluded that there was no interaction between ZnO NPs and PA or LPS on toxicity to HUVECs in vitro. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity, oxidative stress and inflammation induced by ZnO nanoparticles in endothelial cells: interaction with palmitate or lipopolysaccharide

Gong

Liu

et al. 2016

J. Appl. Toxicol.

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“…The expression of VCAM-1, pro-inflammatory cytokines and chemoattractant cytokines, including IL-8 and McP-1, in LPS-induced cells is regulated by the MAPK/IKK/IκB signaling cascade and activation of NF-κB (9,10,32). In addition, interactions with transcription factor binding elements, including NF-κB, can affect the activation of cell adhesion molecules and inflammatory mediators by LPS stimulation (32). In inflammatory conditions, the present study confirmed that CA inhibited the expression of VCAM-1 and pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Cynandioneï¿½A inhibits lipopolysaccharide-induced cell adhesion via suppression of the protein expression of VCAM‑1 in human endothelial cells

et al. 2018

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Cynandione A (CA) is one of the most active compounds in the roots of Cynanchum wilfordii, the extracts of which have been used extensively in East Asia to treat various diseases including anti‑ischemic stroke. In the present study, the anti‑adherent activity of CA in lipopolysaccharide (LPS)‑stimulated human umbilical vascular endothelial cells (HUVECs) was investigated. CA markedly reduced the expression of vascular adhesion molecule‑1 (VCAM‑1) by LPS in HUVECs. The results also demonstrated that CA significantly reduced the expression of pro‑inflammatory and chemoattractant cytokines, including interleukin (IL)‑1β, IL‑6, IL‑8, monocyte chemoattractant protein‑1 and tumor necrosis factor‑α, in LPS‑activated human endothelial cells. CA inhibited the phosphorylation of mitogen‑activated protein kinases, including the extracellular signal‑regulated kinase 1/2 and p38 kinases. It was found that CA decreased the IKK/IκB‑α phosphorylation of inhibitor of nuclear factor (NF)‑κB kinase/inhibitor of NF‑κB‑α, suppressed translocation of the NF‑κB p65 subunit into the nucleus and inhibited the transcriptional activity of NF‑κB. CA also decreased human monocyte cell adhesion to endothelial cells in LPS‑stimulated conditions. These results demonstrated that CA inhibited the protein expression of VCAM‑1 and pro‑inflammatory cytokines by suppressing the transcriptional activity of NF‑κB. The results also suggested that CA may be important in the development of anti‑inflammatory drugs by inhibiting the expression of cell adhesion molecules.

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“…possess various pharmacological effects including antioxidant activity (12), anti-inflammation (13), neuroprotection (14) and the prevention of articular cartilage degeneration (10).…”

Section: Biochanin-a Induces Apoptosis and Suppresses Migration In Famentioning

confidence: 99%

Biochanin-A induces apoptosis and suppresses migration in FaDu human pharynx squamous carcinoma cells

et al. 2017

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The aim of the present study was to investigate biochanin-A-induced anticancer effects and their cellular signaling pathway in FaDu pharyngeal squamous carcinoma cells. Biochanin-A induced cell death through increased cytotoxicity of FaDu cells in a dose- and time-dependent manner. The number of cells with nucleus condensation and the apoptotic population were increased in the FaDu cells stimulated with biochanin-A for 24 h. Furthermore, extrinsic apoptotic factors such as FasL and their downstream target caspase-8 were increased and activated in the FaDu cells treated with biochanin-A in a dose-dependent manner. Moreover, biochanin-A decreased the expression of intrinsic anti-apoptotic factors such as Bcl-2 and Bcl-xL, and increased the level and activation of intrinsic apoptotic factors such as Bad and caspase-9. Finally, biochanin-A induced the activation of caspase-3 and Poly(ADP ribose) polymerase (PARP) in FaDu cells. Our results suggest that biochanin-A-induced apoptosis was mediated by death receptor mediated-extrinsic and mitochondria-dependent intrinsic apoptotic signaling pathways. Biochanin-A also inhibited wound healing migration and proliferation of FaDu cells via the downregulation and inactivation of matrix metalloproteinase-2 and -9 that are mediated by the suppression of p38, mitogen activated protein kinase (MAPK), NF-κB and Akt cellular signaling pathways. Therefore, these data suggest that the biochanin-A may act as a potential chemotherapeutic compound to treat head and neck cancer.

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Biochanin A inhibits lipopolysaccharide-induced inflammation in human umbilical vein endothelial cells

Cited by 50 publications

References 38 publications

Cytotoxicity, oxidative stress and inflammation induced by ZnO nanoparticles in endothelial cells: interaction with palmitate or lipopolysaccharide

Cytotoxicity, oxidative stress and inflammation induced by ZnO nanoparticles in endothelial cells: interaction with palmitate or lipopolysaccharide

Cynandioneï¿½A inhibits lipopolysaccharide-induced cell adhesion via suppression of the protein expression of VCAM‑1 in human endothelial cells

Biochanin-A induces apoptosis and suppresses migration in FaDu human pharynx squamous carcinoma cells

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