Aspirin inhibits LPS-induced macrophage activation via the NF-κB pathway

Liu, Yitong; Fang, Silian; Li, Xiaoyan; Feng, Jie; Du, Juan; Guo, Lijia; Su, Yingying; Zhou, Jian; Ding, Gang; Bai, Yuxing; Wang, Songling; Wang, Hao

doi:10.1038/s41598-017-10720-4

Cited by 73 publications

(75 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Infiltrating macrophages then release proinflammatory cytokines such as TNF-α, IL-1, and interleukin-6 (IL-6), resulting in cytokine release from the infiltrating macrophages and further macrophage recruitment and amplification of the inflammatory response [17]. In addition, TNF-α and NO released by the macrophages can also directly activate the NF-κB pathway (Fig.…”

Section: Inflammation and Ia Pathophysiologymentioning

confidence: 99%

“…Aspirin, a nonselective COX inhibitor, inhibits the NF-κB signaling pathway, decreases macrophage activation, and decreases the release of the proinflammatory cytokines IL-6 and TNF-α (Fig. 3) [17]. Treatment of rodents with the TNF-α inhibitor etanercept slows IA formation which is associated with reduced NF-κB activity and subsequent inhibition of iNOS and MMP expression [18].…”

Section: Evidence That Nsaids Decrease Pgs and Ros In Iamentioning

confidence: 99%

“…iNOS is converted by L-arginine into nitric oxide (NO), a reactive oxygen species. b Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) prevents COX-2 conversion of arachidonic acid and all downstream PGE 2 signaling effects [12, 17, 25, 34, 60]. …”

Section: Inflammation and Ia Pathophysiologymentioning

confidence: 99%

See 2 more Smart Citations

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm

Fisher

Demel

2019

Cerebrovasc Dis Extra

View full text Add to dashboard Cite

Background: Saccular intracranial aneurysms (IAs) are outpouchings of the vessel wall of intracranial arteries. Rupture of IAs results in subarachnoid hemorrhage which is associated with high morbidity and mortality. Surgical interventions, such as clipping and coiling, have associated risks. Currently, there are no proven pharmacological treatments to prevent the growth or rupture of IAs. Infiltration of proinflammatory cytokines in response to increased wall sheer stress is a hallmark of IA. Nonsteroidal anti-inflammatory drugs (NSAIDs) are being investigated as potential therapeutic agents for reduction in growth and/or prevention of IA through inhibition of inflammatory pathways. Summary: This review will discuss the role of NSAIDs in attenuating the inflammation that drives IA progression and rupture. There are two main subtypes of NSAIDs, nonselective COX and selective COX-2 inhibitors, both of which have merit in treating IA. Evidence will be presented which shows that NSAIDs inhibit several key inflammatory mediators involved in IA progression including nuclear factor-κB, tumor necrosis factor-α, and matrix metalloproteinases. In addition, the role of NSAIDs in limiting inflammatory cell adhesion to endothelial cells and attenuating endothelial cell senescence will be discussed. Key Messages: There is an abundance of basic science and preclinical data that support NSAIDs as a promising treatment for IA. Additionally, a combination treatment strategy of low-dose aspirin given concomitantly with a selective COX-2 inhibitor may result in a reduced side effect profile compared to aspirin or selective COX-2 inhibitor use alone. Several large clinical trials are currently planned to further investigate the efficacy of NSAIDs as an effective nonsurgical treatment for IAs.

show abstract

Section: Inflammation and Ia Pathophysiologymentioning

confidence: 99%

Section: Evidence That Nsaids Decrease Pgs and Ros In Iamentioning

confidence: 99%

See 1 more Smart Citation

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm

Fisher

Demel

2019

Cerebrovasc Dis Extra

View full text Add to dashboard Cite

show abstract

“…Besides, pro-inflammatory M1 macrophages have also been demonstrated to facilitate tissue repair. Lipopolysaccharide �LPS� is a well-known factor used to initiate pro-inflammatory responses in macrophages (21). However, LPS has been demonstrated to activate microglia, which perform neuroprotection against experimental brain injury �22�.…”

Section: Discussionmentioning

confidence: 99%

Assessment of para‑inflammation in a wound healing model

et al. 2020

View full text Add to dashboard Cite

A thorough understanding of the inflammatory process has substantial biological and clinical relevance. Para-inflammation has been described as an adaptive response of the immune system to low levels of tissue stress. However, the role of para-inflammation in wound repair requires further investigation. In the present study, the expression levels of several para-inflammation genes were assessed in a murine cutaneous wound healing model. The results revealed that the expression levels of the para-inflammation genes were significantly altered. Among the genes that were examined, the expression levels of solute carrier family 7 member 11 (Slc7a11) paralleled those of the M2 macrophage-associated genes. Further investigation indicated that the Slc7a11 gene and its encoded protein cystine/glutamate transporter exhibited increased expression levels in IL-4-induced M2 macrophages. Notably, the inhibition of para-inflammation by sulindac prolonged wound healing process. The present study indicated that para-inflammation exhibited a protective effect in wound healing and provided new insight for host tissue repair.

show abstract

“…LPS is a well-known stimulant that strongly activates immune system signals and inflammation [9]. Specifically, LPS activates M1 macrophages, which play an important role in secreting inflammatory cytokines and generating reactive oxygen species [10]. Regarding bone biology, LPS stimulation promotes the formation of osteoclasts by increasing receptor activator of NF-kappaB ligand (RANKL) levels or directly stimulating osteoclast progenitor cells [11], leading to bone resorption.…”

Section: Introductionmentioning

confidence: 99%

Releasing Behavior of Lipopolysaccharide from Gelatin Modulates Inflammation, Cellular Senescence, and Bone Formation in Critical-Sized Bone Defects in Rat Calvaria

et al. 2019

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) is a well-known strong inducer of inflammation. However, there is little information regarding how LPS-release behavior affects cellular senescence at the affected area. In this paper, we demonstrate that a vacuum-heating technique (dehydrothermal treatment) can be utilized to prepare an LPS sustained-release gelatin sponge (LS-G). LPS sustained release from gelatin leads to the long-term existence of senescent cells in critical-sized bone defects in rat calvaria. Three types of gelatin sponges were prepared in this study: a medical-grade gelatin sponge with extremely low LPS levels (MG), LS-G, and a LPS rapid-release gelatin sponge (LR-G). Histological (H-E) and immunohistochemical (COX-2, p16, and p21) staining were utilized to evaluate inflammatory reactions and cellular senescence one to three weeks after surgery. Soft X-ray imaging was utilized to estimate new bone formation in the defects. The LR-G led to stronger swelling and COX-2 expression in defects compared to the MG and LS-G at 1 week. Despite a small inflammatory reaction, LS-G implantation led to the long-term existence of senescent cells and hampered bone formation compared to the MG and LR-G. These results suggest that vacuum heating is a viable technique for preparing different types of materials for releasing bacterial components, which is helpful for developing disease models for elucidating cellular senescence and bone regeneration.

show abstract

Aspirin inhibits LPS-induced macrophage activation via the NF-κB pathway

Cited by 73 publications

References 36 publications

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm

Nonsteroidal Anti-Inflammatory Drugs: A Potential Pharmacological Treatment for Intracranial Aneurysm

Assessment of para‑inflammation in a wound healing model

Releasing Behavior of Lipopolysaccharide from Gelatin Modulates Inflammation, Cellular Senescence, and Bone Formation in Critical-Sized Bone Defects in Rat Calvaria

Contact Info

Product

Resources

About