Effect of Aspirin on Fractalkine in Rats with Pulmonary Embolism

Wang, Li‐Chieh; Wu, J-N; Xia, G-L; Mao, Wu; Ying, R.; Huang, LQ; Jiang, R-L

doi:10.4314/tjpr.v13i5.15

Cited by 6 publications

(9 citation statements)

References 13 publications

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“…CX3CL1 is important in the recruitment of inflammatory cells into the vascular wall in endothelial cell injury (12,13). Previous studies have reported that TNF-α stimulates the CX3CL1/CX3CR1 inflammatory signaling pathway, whereas our previous studies revealed that the expression levels of TNF-α, CX3CL1 and CX3CR1 were significantly increased in rats with pulmonary embolism (3,14). Certain studies have reported that the presence and the stimulation of the CX3CL1 receptor, CX3CR1, is correlated with the reduced release of IL-1β and TNF-α (15,16).…”

Section: Discussioncontrasting

confidence: 62%

“…Our previous studies demonstrated that a wide range of inflammatory responses, including the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-8, the irregular chemokine CX3C chemokine ligand 1 (CX3CL1) and its receptor CX3C chemokine receptor 1 (CX3CR1) were found in an APE rat model. In addition, the level of CX3CL1 was shown to positively correlate with the level of TNF-α (3,4). It was also found that lipopolysaccharide (LPS) can induce the expression of nuclear factor (NF)-κB and CX3CL1 in human bronchial epithelial cells (5), and it was found that aspirin improved the pathological changes in rats with APE via the CX3CL1/CX3CR1 signaling pathway (3,4).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the level of CX3CL1 was shown to positively correlate with the level of TNF-α (3,4). It was also found that lipopolysaccharide (LPS) can induce the expression of nuclear factor (NF)-κB and CX3CL1 in human bronchial epithelial cells (5), and it was found that aspirin improved the pathological changes in rats with APE via the CX3CL1/CX3CR1 signaling pathway (3,4). Based on these findings, adenovirus vectors carrying CX3CL1-short hairpin (sh)RNA and CX3CL1-overexpression vectors were constructed in the present study to identify the thrombus-induced inflammatory response involving lung microvascular endothelial cells (LMVECs) at the cellular level, and examine the intervention effect of aspirin.…”

Section: Introductionmentioning

confidence: 99%

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Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Wang

Ying²,

Jiang

et al. 2018

Int J Mol Med

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The purpose of the present study was to examine whether aspirin interferes with the inflammatory response in a thrombus-stimulated lung microvascular endothelial cell (LMVEC) model. The LMVECs were randomly divided into eight groups: Normal group (group N), model group (group M), model + ASP group (group M+A), model+CX3CL1-short hairpin (sh)RNA group (group M+SH), model + CX3CL1-overexpression vector group (group M+CX3), model + ASP + shRNA group (group M+A+SH), model + ASP + CX3CL1-overexpression vector group (group M+A+CX3), and normal + virus control group (group N+V). The endothelial cells were cultured, and a thrombus was added to the cells. Briefly, 12 h following the precipitation of the thrombus, data from ELISA, reverse transcription-quantitative polymerase chain reaction analysis and confocal microscopy revealed that the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, CX3C chemokine ligand 1 (CX3CL1), CX3C chemokine receptor 1 (CX3CR1) and nuclear factor-κB (NF-κB) in group M were increased, compared with those in group N (P<0.01). These levels, with the exception of TNF-α, were significantly lower in group M+SH, compared with those in group M (P<0.01). Furthermore, the levels of IL-6 in groups M+A, M+CX3 and M+A+CX3 were decreased, compared with those in group M (P<0.01); the level of TNF-α in group M+A+SH was decreased, compared with that in group M (P<0.01); the level of CX3CR1 waslower in groups M+A and M+A+SH, compared with that in group M (P<0.01), and the level of NF-κB in group M+SH was decreased, compared with the level in group M and group M+A (P<0.05). In conclusion, the thrombus-stimulated LMVEC model exhibited induced production of TNF-α, IL-6, CX3CL, CX3CR1, NF-κB and intercellular adhesion molecule-1. Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-κB, IL-6 and TNF-α were partly inhibited by aspirin.

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Section: Discussioncontrasting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Wang

Ying²,

Jiang

et al. 2018

Int J Mol Med

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“…Firstly, although inflammatory reactions contribute to the aggravation of thrombus formation, the relationship between the two factors needs to be further explored. Secondly, only five groups of rats have been established in this study, but aspirin as a control group was not established as in our previous study [11–13]. This was done in order to decrease the unnecessary animal sacrifices.…”

Section: Discussionmentioning

confidence: 99%

“…Thromboxane A2 (TXA2, Youersheng Science and Technology Co. Ltd., Wuhan, China), brain natriuretic peptide (BNP, Youersheng Science and Technology Co. Ltd., Wuhan, China), troponin I gene (TNNI3, Youersheng Science and Technology Co. Ltd., Wuhan, China), and D-Dimer (D2D, Youersheng Science and Technology Co. Ltd., Wuhan, China) levels in the rat serum were detected by a double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). The specific experimental procedures used are based on our previously reported studies [11–13]. Pulmonary pathology examined was as follows: after the examination of the gross pathology of the lung, lung tissue was fixed by 10% formalin for 24 h. The paraffin-embedded sections were prepared and then stained with a hematoxylin-eosin (H&E) reagent.…”

Section: Methodsmentioning

confidence: 99%

Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

Shi

Zhang

Cai

et al. 2018

Journal of Immunology Research

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Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

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Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-κB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells

et al. 2015

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This study focused on the effects of aspirin on lipopolysaccharide (LPS)-induced expression of phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt), extracellular signal-regulated protein kinase (ERK), nuclear factor-κB (NF-κB), CX3CL1, and MMPs in human bronchial epithelial cells. Human bronchial epithelial cells were seeded in six-well plates. After 24 h, the cells were classified into six groups: control blank (CK) group; LPS group; PD98059 (ERK inhibitor) (PD) group, treated with LPS + ERK inhibitor; LY294002(PI3K/Akt inhibitor) (LY) group, treated with LPS + PI3K/Akt inhibitor; Aspirin (Asp) group, treated with LPS + aspirin; and Pyrrolidinedithiocarbamic acid (PDTC) group, treated with LPS + NF-κB inhibitor. After 4-h treatment, the cells were harvested. Western blot analysis was performed to detect the expression of PI3K/Akt, ERK, NF-κB, and CX3CL1. Real-time quantitative PCR (RT-qPCR) was used to determine the gene expression of MMP-7, MMP-9, and MMP-12. Compared to the CK group, expression of PI3K/Akt, ERK, NF-κB, and CX3CL1 was significantly increased in the LPS group (P < 0.05). When compared to the LPS group, expression of PI3K/Akt, ERK, NF-κB, and CX3CL1 was significantly decreased in the PD group, PDTC group, and Asp group (P < 0.05). In addition, expression of NF-κB in the LY group was significantly reduced by comparison with the LPS group (P < 0.05). RT-qPCR: When compared to the LPS group, expression of MMP-7 and MMP-12 was significantly decreased in Asp group (P < 0.05). Expression of MMP-12 was significantly reduced in LY group (P < 0.05). LPS-ERK, NF-κB-PI3K/Akt, and CX3CL1 signal pathways exist in human bronchial epithelial cells. The PI3K/Akt inhibitor repressed expression of MMP-12. Aspirin inhibited LPS-induced expression of PI3K, Akt, ERK, NF-κB, CX3CL1, MMP-7, and MMP-12 in human bronchial epithelial cells.

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Effect of Aspirin on Fractalkine in Rats with Pulmonary Embolism

Abstract: Purpose: To investigate the effect of aspirin on fractalkine (FKN) in rats with pulmonary embolism (PE and FKN.

Cited by 6 publications

References 13 publications

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Aspirin modulates the inflammatory response in a thrombus‑stimulated LMVEC model

Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response

Aspirin Inhibits LPS-Induced Expression of PI3K/Akt, ERK, NF-κB, CX3CL1, and MMPs in Human Bronchial Epithelial Cells

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