Sinomenine suppresses TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells

Huang, Junshen; Lin, Zhuofeng; Luo, Meiling; Lu, Cuihua; Kim, Michelle H.; Yu, Buyun; J, Gu

doi:10.1016/j.jep.2007.07.036

Cited by 15 publications

(12 citation statements)

References 19 publications

(22 reference statements)

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“…Chinese medical practitioners have been using this plant to treat various rheumatic and arthritic diseases for over hundreds years in China. Sinomenine was shown to inhibit TNF-␣-induced VCAM-1 expression in human umbilical vein endothelial cells (Huang et al, 2007). In another study, sinomenine was found to down regulate the mRNA expression of inflammatory cytokines TNF-␣ and IL-1␤ by inhibiting the NF-B binding activity and cytokine expression of macrophages and synoviocytes in adjuvant arthritis rats (Wang et al, 2005).…”

Section: Discussionmentioning

confidence: 97%

Anti-inflammatory activities of Chinese herbal medicine sinomenine and Liang Miao San on tumor necrosis factor-α-activated human fibroblast-like synoviocytes in rheumatoid arthritis

Chen

Wong

Leung

et al. 2011

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 97%

Anti-inflammatory activities of Chinese herbal medicine sinomenine and Liang Miao San on tumor necrosis factor-α-activated human fibroblast-like synoviocytes in rheumatoid arthritis

Chen

Wong

Leung

et al. 2011

Journal of Ethnopharmacology

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“…Levels of mRNA of human VCAM-1 and actin were measured by quantitative real-time RT-PCR using gene-specific primers (LightCycler, Roche) with SYBR green. Primers for actin were from [15] and VCAM-1 from [16]. Reactions were incubated at 95°C at 5 min before thermal cycling at 95°C for 15 s, 60°C for 5 s, and 72°C for 10 s. Samples were prepared in triplicates and transcript expression was calculated by comparing the number of thermal cycles that were necessary to produce threshold amounts of product as described [17] and normalized by β-actin.…”

Section: Methodsmentioning

confidence: 99%

Anti-Inflammatory Effect of Targeted Delivery of SOD to Endothelium: Mechanism, Synergism with NO Donors and Protective Effects In Vitro and In Vivo

et al. 2013

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Pro-inflammatory activation of vascular endothelium is implicated in pathogenesis of severe conditions including stroke, infarction and sepsis. We have recently reported that superoxide dismutase (SOD) conjugated with antibodies (Ab/SOD) that provide targeted delivery into endothelial endosomes mitigates inflammatory endothelial activation by cytokines and agonists of Toll-like receptors (TLR). The goal of this study was to appraise potential utility and define the mechanism of this effect. Ab/SOD, but not non-targeted SOD injected in mice alleviated endotoxin-induced leukocyte adhesion in the cerebral vasculature and protected brain from ischemia-reperfusion injury. Transfection of endothelial cells with SOD, but not catalase inhibited NFκB signaling and expression of Vascular Cell Adhesion Molecule-1 induced by both cytokines and TLR agonists. These results affirmed that Ab/SOD-quenched superoxide anion produced by endothelial cells in response to proinflammatory agents mediates NFκB activation. Furthermore, Ab/SOD potentiates anti-inflammatory effect of NO donors in endothelial cells in vitro, as well as in the endotoxin-challenged mice. These results demonstrate the central role of intracellular superoxide as a mediator of pro-inflammatory activation of endothelium and support the notion of utility of targeted interception of this signaling pathway for management of acute vascular inflammation.

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“…The remaining cells were > 90% neutrophils as assessed by microscopic evaluation. Neutrophils were stimulated with LPS (100 ng/ml) [32], and SIN (1 mol/L) [33] was added 30 minutes before LPS treatment. To detect the downstream signaling, 10 µmol/L of N-[2-[[3-(4-bromophenyl)-2-prope-nyl]amino]ethyl]-5-isoquinolinesulfonamide dihydrate dihydrochloride (H-89, Calbiochem, Germany) [34], an inhibitor of protein kinase A (PKA), was used.…”

Section: Methodsmentioning

confidence: 99%

Sinomenine Protects against Lipopolysaccharide-Induced Acute Lung Injury in Mice via Adenosine A2A Receptor Signaling

Zhao

Xie

et al. 2013

PLoS ONE

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Sinomenine (SIN) is a bioactive alkaloid extracted from the Chinese medicinal plant Sinomenium acutum, which is widely used in the clinical treatment of rheumatoid arthritis (RA). However, its role in acute lung injury (ALI) is unclear. In this study, we investigate the role of SIN in lipopolysaccharide (LPS)-induced ALI in mice. After ALI, lung water content and histological signs of pulmonary injury were attenuated, whereas the PaO2/FIO2 (P/F) ratios were elevated significantly in the mice pretreated with SIN. Additionally, SIN markedly inhibited inflammatory cytokine TNF-α and IL-1β expression levels as well as neutrophil infiltration in the lung tissues of the mice. Microarray analysis and real-time PCR showed that SIN treatment upregulated adenosine A2A receptor (A2AR) expression, and the protective effect of SIN was abolished in A2AR knockout mice. Further investigation in isolated mouse neutrophils confirmed the upregulation of A2AR by SIN and showed that A2AR-cAMP-PKA signaling was involved in the anti-inflammatory effect of SIN. Taken together, these findings demonstrate an A2AR-associated anti-inflammatory effect and the protective role of SIN in ALI, which suggests a potential novel approach to treat ALI.

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Sinomenine suppresses TNF-α-induced VCAM-1 expression in human umbilical vein endothelial cells

Cited by 15 publications

References 19 publications

Anti-inflammatory activities of Chinese herbal medicine sinomenine and Liang Miao San on tumor necrosis factor-α-activated human fibroblast-like synoviocytes in rheumatoid arthritis

Anti-inflammatory activities of Chinese herbal medicine sinomenine and Liang Miao San on tumor necrosis factor-α-activated human fibroblast-like synoviocytes in rheumatoid arthritis

Anti-Inflammatory Effect of Targeted Delivery of SOD to Endothelium: Mechanism, Synergism with NO Donors and Protective Effects In Vitro and In Vivo

Sinomenine Protects against Lipopolysaccharide-Induced Acute Lung Injury in Mice via Adenosine A2A Receptor Signaling

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