Ohioensin F suppresses TNF-α-induced adhesion molecule expression by inactivation of the MAPK, Akt and NF-κB pathways in vascular smooth muscle cells

Byeon, Hye-Eun; Um, Sung Hee; Yim, Joung Han; Lee, Hong Kum; Pyo, Suhkneung

doi:10.1016/j.lfs.2011.12.017

Cited by 22 publications

(16 citation statements)

References 46 publications

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“…NF-κB plays a key role in regulating heat-killed S. aureus-induced VCAM-1 expression NF-κB has been shown to regulate VCAM-1 expression in vascular smooth muscle cells [1]. We used an NF-κB inhibitor (Bay11-7082) and p65 siRNA to observe whether NF-κB was involved in heat-killed S. aureus-induced VCAM-1 expression.…”

Section: Resveratrol Inhibits Heat-killed S Aureus-induced Vcam-1 Exmentioning

confidence: 99%

“…Staphylococcus aureus is a bacterium that is a member of the Firmicutes, and is frequently found in the human respiratory tract [1]. LTA (lipoteichoic acid), a cell wall component of Grampositive bacteria, functions as an adhesion molecule to facilitate the binding of bacteria to cells, colonization and invasion [2].…”

Section: Introductionmentioning

confidence: 99%

“…Up-regulation of VCAM-1 by LPS has been shown to be mediated through activation of the TLR4/MyD88-dependent p38 MAPK (mitogen-activated protein kinase) pathway [9]. In addition, MAPKs, Akt and NF-κB (nuclear factor κB) have been shown to regulate VCAM-1 expression [1]. Sawa et al [10] has shown leucocyte adhesion molecule and chemokine production through LTA recognition by TLR2.…”

Section: Introductionmentioning

confidence: 99%

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Resveratrol inhibitsStaphylococcus aureus-induced TLR2/MyD88/NF-κB-dependent VCAM-1 expression in human lung epithelial cells

et al. 2014

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Staphylococcus aureus is the most commonly found Gram-positive bacterium in patients admitted to intensive-care units, causing septicaemia or pneumonia. S. aureus is considered to play an important role in the induction of cell adhesion molecules. Resveratrol, a compound found in the skins of red fruits, may inhibit the inflammatory signalling pathways involved in lung diseases. In the present paper, we have shown that resveratrol reduced S. aureus-mediated VCAM-1 (vascular cell adhesion molecule-1) expression in HPAEpiCs (human lung epithelial cells) and lungs of mice. In an in vivo study, we have shown that resveratrol inhibited S. aureus-induced pulmonary haematoma and leucocyte count in BAL (bronchoalveolar lavage) fluid in mice. In an in vitro study, we observed that resveratrol attenuated S. aureus-induced TLR2 (Toll-like receptor 2), MyD88 (myeloid differentiation factor 88) and PI3K (phosphoinositide 3-kinase) complex formation. S. aureus stimulated Akt, JNK1/2 (c-Jun N-terminal kinase 1/2) and p42/p44 MAPK (mitogen-activated protein kinase) phosphorylation, which were inhibited by resveratrol. In addition, S. aureus induced IκB (inhibitor of nuclear factor κB) α and NF-κB (nuclear factor κB) p65 phosphorylation and NF-κB p65 translocation, which were reduced by resveratrol. Finally, we found that S. aureus induced NF-κB and p300 complex formation and p300 phosphorylation, which were inhibited by resveratrol. Thus resveratrol functions as a suppressor of S. aureus-induced inflammatory signalling not only by inhibiting VCAM-1 expression, but also by reducing TLR2-MyD88-PI3K complex formation and Akt, JNK1/2, p42/p44 MAPK, p300 and NF-κB activation in HPAEpiCs.

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Section: Resveratrol Inhibits Heat-killed S Aureus-induced Vcam-1 Exmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Resveratrol inhibitsStaphylococcus aureus-induced TLR2/MyD88/NF-κB-dependent VCAM-1 expression in human lung epithelial cells

et al. 2014

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“…NF-κB with a sequence-specific dimeric structure is an important type of transcription factor existing widely in mammalian cells, which can bind specifically to a variety of cellular gene-promoter and -enhancer sequences (Kwak et al, 2011;Yamanaka et al, 2011;Byeon et al, 2012). Its activation, as a regulator of inflammation and oxidative stress reaction, is also involved in the process of cell proliferation and apoptosis (Goldin et al, 2006;GratasDelamarche et al, 2014).…”

Section: Effect Of Naringin On P65 Protein Expression In Gp120-treatementioning

confidence: 99%

“…NF-κB plays a critical role in immune response, inflammatory reaction, and cell growth regulation by controlling the expression of various crucial cytokines, adhesion molecules, and chemokines (Kwak et al, 2011;Yamanaka et al, 2011;Byeon et al, 2012). Moreover, NF-κB is also the main regulator of inflammation and oxidative stress reactions (Goldin et al, 2006;Gratas-Delamarche et al, 2014), and its activation is also involved in cell proliferation and apoptosis.…”

Section: Dissussionmentioning

confidence: 99%

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

Chen

Qin

et al. 2016

Genet. Mol. Res.

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ABSTRACT. This study was aimed at exploring the effects of P2X 7 receptors on gp120-induced injury and naringin's protective effects against gp120-induced injury in BV2 microglia. BV2 microglia injury model was established by gp120 treatment and MTS assay was used to verify whether naringin has a cell-protective effect against gp120-induced injury. Changes in P2X 7 receptor expression were assayed using RT-PCR, qPCR, and western blot. Results showed that the ODs of the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.91 ± 0.10, 0.71 ± 0.09, 0.83 ± 0.10, and 0.83 ± 0.10, respectively. Compared to the control group, the gp120 group showed a significantly decreased cell survival rate. Cell survival rates of the gp120+naringin group increased significantly compared to those of the gp120 group, while no difference was observed when compared to the gp120+BBG group. The relative P2X 7 mRNA expression levels in the Ctrl, gp120, gp120+naringin, and gp120+BBG groups were 0.73 ± 0.06, 1.05 ± 0.06, 0.78 ± 0.05, and 0.81 ± 0.04, respectively. The corresponding P2X 7 protein expression levels were 0.46 ± 0.04, 0.79 ± 0.04, 0.38 ± 0.07, and 0.42 ± 0.06. P2X 7 mRNA and protein expression in the gp120 group increased significantly compared to those in the control group, and declined in the gp120+naringin group compared to those in the gp120 group. Therefore, P2X 7 receptors might be involved in gp120-induced injury in BV2 microglia, and naringin might play a protective role by inhibiting the up-regulated expression of P2X 7 receptors.

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The P2X7 Receptor Involved in gp120-Induced Cell Injury in BV2 Microglia

Chen

Qin

et al. 2016

Inflammation

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This study was aimed at exploring the effects of P2X7 receptor on BV2 microglia cell injury induced by glycoprotein gp120 (gp120) and its underlying mechanisms. We used the MTS method to study the influence of different gp120 concentrations on BV2 microglia cells, and to test the degree of cell injury in each gp120 treatment group; quantitative real-time PCR (qPCR) and Western blot were used to detect the P2X7 mRNA and receptor protein expressions. Immunocytochemistry and Western blot were used to detect the P2X7 receptor expression and P65 NF-κB, respectively. We also measured the content of TNFα, IL-1β, nitric oxide (NO) and reactive oxygen species (ROS). We found that the cell survival rate generally decreased as gp120 concentration increased, and the cell survival rate of the gp120 + Brilliant Blue G (BBG) group was higher than that of the gp120 group. Western blot and qPCR results showed that the expressions of P2X7 receptor protein and mRNA were positively dose-dependent with gp120 concentration; the results of immunocytochemistry and Western blot showed that the expressions of P2X7 receptor and P65 NF-κB in the gp120 group increased significantly compared to those of the control (Ctrl) group, but those in the gp120+BBG group decreased. Taken together, these results confirmed that the P2X7 receptor is involved in gp120-induced BV2 microglial cell injury and that the underlying mechanism may be associated with the over-activation of microglia caused by P2X7 receptor up-regulation, which leads to abundant release of inflammatory factors which exert toxic effects on the cells.

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Ohioensin F suppresses TNF-α-induced adhesion molecule expression by inactivation of the MAPK, Akt and NF-κB pathways in vascular smooth muscle cells

Cited by 22 publications

References 46 publications

Resveratrol inhibitsStaphylococcus aureus-induced TLR2/MyD88/NF-κB-dependent VCAM-1 expression in human lung epithelial cells

Resveratrol inhibitsStaphylococcus aureus-induced TLR2/MyD88/NF-κB-dependent VCAM-1 expression in human lung epithelial cells

Protective effects of naringin against gp120-induced injury mediated by P2X7 receptors in BV2 microglial cells

The P2X7 Receptor Involved in gp120-Induced Cell Injury in BV2 Microglia

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