Ceftiofur attenuates lipopolysaccharide-induced acute lung injury

Chu, Xiao; Song, Keji; Xu, Kan; Zhang, Xiaozhe; Zhang, Xuemei; Song, Yu; Wang, Dacheng; Liu, Songcai; Deng, Xuming

doi:10.1016/j.intimp.2010.02.010

Cited by 19 publications

(17 citation statements)

References 27 publications

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“…Neutrophils excrete MPO in the extracellular medium, bringing about an accumulation of HOCl and several other reactive oxygen derivatives and leading to an oxidative modification of proteins or cellular structures [22,23]. Our present data illustrated increased MPO activity in the lung tissue in LPS model, which was consistent with the histopathological changes of leukocyte infiltration, while such increase was significantly reduced by three doses of ruscogenin (Fig.…”

Section: Discussionsupporting

confidence: 88%

Ruscogenin inhibits lipopolysaccharide-induced acute lung injury in mice: Involvement of tissue factor, inducible NO synthase and nuclear factor (NF)-κB

Sun

Chen

Gao

et al. 2012

International Immunopharmacology

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Section: Discussionsupporting

confidence: 88%

Ruscogenin inhibits lipopolysaccharide-induced acute lung injury in mice: Involvement of tissue factor, inducible NO synthase and nuclear factor (NF)-κB

Sun

Chen

Gao

et al. 2012

International Immunopharmacology

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“…LPS induces rapid phosphorylation of ERK1/2, JNK, and p38 kinase in a macrophage cell line (RAW264.7), and ceftiofur treatment impairs phosphorylation of these molecules in a dose-dependent manner [14] . This in vitro effect of ceftiofur in cell culture was previously confirmed by LPS-induced endotoxemia and acute lung injury animal models in mice in vivo as well [15,16] . We also examined that, parallel to its inhibitory effect on increased protein expression in the spinal cord, ceftiofur significantly attenuated clinical signs in a rat neuropathic pain model in a dose-dependent manner.…”

Section: Discussionsupporting

confidence: 62%

“…Ceftiofur is a third-generation cephalosporin derivative and inhibits lipopolysaccharide (LPS)-induced production of TNF-α, IL-1β, and IL-6 in mouse macrophages through the inhibition of the LPSinduced activation of MAPK signaling and LPS-induced translocation of NF-κB from the cytoplasm to the nucleus [14] . It also has beneficial effects on LPS-induced endotoxemia and acute lung injury in mice through modulation of cytokine levels [15,16] .…”

mentioning

confidence: 99%

Effect of Ceftiofur on Hyperalgesia and Allodynia in a Rat Neuropathic Pain Model: The Role of Immune Processes

Önal¹,

Coskunsever²,

Çelenk³

et al. 2017

Neuroimmunomodulation

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Objective: Inflammatory and immune mechanisms play important roles in the pathogenesis of neuropathic pain. Ceftiofur, a third-generation cephalosporin, has anti-inflammatory effects by inhibiting tumor necrosis factor (TNF)-α, interleukin (IL)-1β, nuclear factor (NF)-κB, and mitogen-activated protein kinase (MAPK) signaling. This study aimed to investigate the effect of ceftiofur on hyperalgesia and allodynia in neuropathic rats and to define the possible contribution of immune mechanisms to this effect. Methods: A neuropathic pain model was performed by ligating the right sciatic nerve. Mechanic hyperalgesia and allodynia were measured using an analgesia meter and dynamic plantar esthesiometer, respectively. Following sciatic nerve ligation, ceftiofur was administered intraperitoneally (10 and 20 mg/kg/day) for 14 days. The control group received saline. Pain thresholds were recorded pre- and postoperatively on days 3, 7, 10, and 14. Protein was extracted from lumbar spinal cord tissue on day 14, and TNF-α, IL-1β, p65 NF-κB, p38 MAPK, and inducible nitric oxide synthase (iNOS) were evaluated by Western blotting. Results: Neuropathic rats showed decreased pain thresholds in analgesia meter and esthesiometer measurements. Ceftiofur 20 mg/kg/day significantly alleviated hyperalgesia, but not allodynia, and the increased iNOS and IL-1β expression was attenuated in neuropathic rats at both doses while decreasing p38 MAPK expression only at 20 mg/kg/day. TNF-α and p65 NF-κB expression remained unchanged 14 days after surgery. Conclusions: Ceftiofur has anti-inflammatory effects by decreasing iNOS, IL-1β, and p38 MAPK expression in lumbar spinal cord, and treatment of neuropathic rats with repeated doses of ceftiofur for 14 days results in antihyperalgesic effects.

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“…Fibroblast-secreted SDF-1 plays a key role in maintaining chronic inflammation 18, 19, and TNF-α is the earliest and primary endogenous mediator of inflammatory response 20. For this reason, we tested whether SDF-1 could also directly stimulate pro-inflammatory response through evaluation of the secretion of TNF-α.…”

Section: Resultsmentioning

confidence: 99%

SDF-1 in Mammary Fibroblasts of Bovine with Mastitis Induces EMT and Inflammatory Response of Epithelial Cells

Yang

et al. 2017

Int. J. Biol. Sci.

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Fibroblasts constitute the majority of the stromal cells within bovine mammary gland, yet the functional contributions of these cells to mastitis and fibrosis and the mechanism are poorly understood. In this study, we demonstrate that inflammation-associated fibroblasts (INFs) extracted from bovine mammary glands with clinical mastitis had different expression pattern regarding to several extracellular matrix (ECM) proteins, chemokines and cytokines compared to normal fibroblasts (NFs) from dairy cows during lactation. The INFs induced epithelial-mesenchymal transition (EMT) and inflammatory responses of mammary epithelial cells in a vitro co-culture model. These functional contributions of INFs to normal epithelial cells were mediated through their ability to secrete stromal cell-derived factor 1 (SDF-1). SDF-1 was highly secreted/expressed by INFs, lipopolysaccharide (LPS) -treated NFs, lipoteichoic acid (LTA) -treated NFs, as well as mastitic tissue compared to their counterparts. Exogenous SDF-1 promoted EMT on epithelial cells through activating NF-κB pathway, induced inflammation response and inhibited proliferation of epithelial cells. In addition, SDF-1 was able to induce mastitis and slight fibrosis of mouse mammary gland, which was attenuated by a specific inhibitor of the receptor of SDF-1. Our findings indicate that stromal fibroblasts within mammary glands with mastitis contribute to EMT and inflammatory responses of epithelial cells through the secretion of SDF-1, which could result in the inflammation spread and fibrosis within mammary gland.

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Ceftiofur attenuates lipopolysaccharide-induced acute lung injury

Cited by 19 publications

References 27 publications

Ruscogenin inhibits lipopolysaccharide-induced acute lung injury in mice: Involvement of tissue factor, inducible NO synthase and nuclear factor (NF)-κB

Ruscogenin inhibits lipopolysaccharide-induced acute lung injury in mice: Involvement of tissue factor, inducible NO synthase and nuclear factor (NF)-κB

Effect of Ceftiofur on Hyperalgesia and Allodynia in a Rat Neuropathic Pain Model: The Role of Immune Processes

SDF-1 in Mammary Fibroblasts of Bovine with Mastitis Induces EMT and Inflammatory Response of Epithelial Cells

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