Methyl-β-cyclodextrin suppresses the monocyte-endothelial adhesion triggered by lipopolysaccharide (LPS) or oxidized low-density lipoprotein (oxLDL)

Chen, Guo; Zhou, Yun; Zhang, Wendiao; Qin, Ying; Wei, Bo; Sun, Yanan; Chen, Yong

doi:10.1080/13880209.2021.1953540

Cited by 13 publications

(10 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…also indicated that Vγ4 + γδ T cells secreted IL-17A via regulating the PI3K/Akt/mTOR axis [ 60 ]. As was reported, LCD strongly modified NF-κB or the mTOR signaling pathway in different cell environments, including monocyte-endothelial adhesion [ 61 ], breast cancer cells’ resistance to TRAIL [ 62 ] and lipid raft-dependent activation in bronchial epithelial cells [ 63 ]. Hence, we inferred that LCD nanoparticles probably influence IL-17A secretion via signaling pathways mentioned above in Vγ4 + γδ T cells, which needs to be further investigated.…”

Section: Discussionmentioning

confidence: 91%

Luminol-conjugated cyclodextrin biological nanoparticles for the treatment of severe burn-induced intestinal barrier disruption

Song,

Li,

et al. 2024

Burns &Amp; Trauma

View full text Add to dashboard Cite

Background The breakdown of intestinal barrier integrity occurs after severe burn injury and is responsible for the subsequent reactions of inflammation and oxidative stress. A new protective strategy for the intestinal barrier is urgently needed due to the limitations of the traditional methods. Recently, the application of nanoparticles has become one of the promising therapies for many inflammation-related diseases or oxidative damage. Herein, we developed a new anti-inflammatory and antioxidant nanoparticle named luminol-conjugated cyclodextrin (LCD) and aimed to evaluate its protective effects in severe burn-induced intestinal injury. Methods First, LCD nanoparticles, engineered with covalent conjugation between luminol and β-cyclodextrin (β-CD), were synthesized and examined. Then a mouse burn model was successfully established before the mouse body weight, intestinal histopathological manifestation, permeability, tight junction (TJ) expression and pro-inflammatory cytokines were determined in different groups. The proliferation, apoptosis, migration and reactive oxygen species (ROS) of intestinal epithelial cells (IECs) were assessed. Intraepithelial lymphocytes (IELs) were isolated and cultured for analysis by flow cytometry. Results LCD nanoparticle treatment significantly relieved the symptoms of burn-induced intestinal injury in the mouse model, including body weight loss and intestinal permeability abnormalities. Moreover, LCD nanoparticles remarkably recovered the mechanical barrier of the intestine after severe burn, renewed TJ structures, promoted IEC proliferation and migration, and inhibited IEC apoptosis. Mechanistically, LCD nanoparticles dramatically alleviated pro-inflammation factors (tumor necrosis factor-α, IL-17A) and ROS accumulation, which could be highly involved in intestinal barrier disruption. Furthermore, an increase in IL-17A and the proportion of IL-17A+Vγ4+ γδ T subtype cells was also observed in vitro in LPS-treated Vγ4+ γδ T cells, but the use of LCD nanoparticles suppressed this increase. Conclusions Taken together, these findings demonstrate that LCD nanoparticles have the protective ability to ameliorate intestinal barrier disruption and provide a therapeutic intervention for burn-induced intestinal injury.

show abstract

Section: Discussionmentioning

confidence: 91%

Luminol-conjugated cyclodextrin biological nanoparticles for the treatment of severe burn-induced intestinal barrier disruption

Song,

Li,

et al. 2024

Burns &Amp; Trauma

View full text Add to dashboard Cite

show abstract

“…This shows that with an oxLDL target these agents were not acting primarily by disrupting the oxLDL through their action as cholesterol solvents, because the results were very similar with both targets. Previously, MCD had also been shown to cause endothelial cells to reduce adhesion molecule expression and the adhesion of monocytes [ 58 ], and to inhibit monocyte adhesion to endothelial cells stimulated with LPS or oxLDL [ 59 ], although the involvement of lipid rafts in these events was not investigated. In addition, the sensitive disruption shown here of adhesion to FN, which binds primarily to α 5 β 1 integrin, confirms that raft structure is required for integrin mediated adhesion, as determined previously [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

Monocytic Cell Adhesion to Oxidised Ligands: Relevance to Cardiovascular Disease

et al. 2022

View full text Add to dashboard Cite

Atherosclerosis, the major cause of vascular disease, is an inflammatory process driven by entry of blood monocytes into the arterial wall. LDL normally enters the wall, and stimulates monocyte adhesion by forming oxidation products such as oxidised phospholipids (oxPLs) and malondialdehyde. Adhesion molecules that bind monocytes to the wall permit traffic of these cells. CD14 is a monocyte surface receptor, a cofactor with TLR4 forming a complex that binds oxidised phospholipids and induces inflammatory changes in the cells, but data have been limited for monocyte adhesion. Here, we show that under static conditions, CD14 and TLR4 are implicated in adhesion of monocytes to solid phase oxidised LDL (oxLDL), and also that oxPL and malondialdehyde (MDA) adducts are involved in adhesion to oxLDL. Similarly, monocytes bound to heat shock protein 60 (HSP60), but this could be through contaminating lipopolysaccharide. Immunohistochemistry on atherosclerotic human arteries demonstrated increased endothelial MDA adducts and HSP60, but endothelial oxPL was not detected. We propose that monocytes could bind to MDA in endothelial cells, inducing atherosclerosis. Monocytes and platelets synergized in binding to oxLDL, forming aggregates; if this occurs at the arterial surface, they could precipitate thrombosis. These interactions could be targeted by cyclodextrins and oxidised phospholipid analogues for therapy.

show abstract

“…A study on pancreatic and glioma cancer cells showed that methyl-β-Cyclodextrin depletes cholesterol in cell membranes and destroy lipid rafts, leading to an increase in CD44 extracellular lipid distribution, and promoting CD44 related tumor metastasis mediated by ADAM-10, a metalloproteinase ( 72 ). methyl-β-Cyclodextrin can also inhibit cell growth and cell cycle arrest through the expression of cyclin A and D1 mediated by prostaglandin E ( 2 ) independent pathway ( 134 ), and inhibit endothelial adhesion of monocytes induced by lipopolysaccharide or oxidized low-density lipoprotein ( 135 ). The above indicates methyl β-Cyclodextrin may become a new drug for tumor therapy.…”

Section: Potential Role Of Lipid Metabolism Related Drugs In Tumorsmentioning

confidence: 99%

Association between abnormal lipid metabolism and tumor

Wang

et al. 2023

Front. Endocrinol.

View full text Add to dashboard Cite

Metabolic Reprogramming is a sign of tumor, and as one of the three major substances metabolism, lipid has an obvious impact. Abnormal lipid metabolism is related to the occurrence of various diseases, and the proportion of people with abnormal lipid metabolism is increasing year by year. Lipid metabolism is involved in the occurrence, development, invasion, and metastasis of tumors by regulating various oncogenic signal pathways. The differences in lipid metabolism among different tumors are related to various factors such as tumor origin, regulation of lipid metabolism pathways, and diet. This article reviews the synthesis and regulatory pathways of lipids, as well as the research progress on cholesterol, triglycerides, sphingolipids, lipid related lipid rafts, adipocytes, lipid droplets, and lipid-lowering drugs in relation to tumors and their drug resistance. It also points out the limitations of current research and potential tumor treatment targets and drugs in the lipid metabolism pathway. Research and intervention on lipid metabolism abnormalities may provide new ideas for the treatment and survival prognosis of tumors.

show abstract

Methyl-β-cyclodextrin suppresses the monocyte-endothelial adhesion triggered by lipopolysaccharide (LPS) or oxidized low-density lipoprotein (oxLDL)

Abstract: Chen (2021) Methyl-β-cyclodextrin suppresses the monocyte-endothelial adhesion triggered by lipopolysaccharide (LPS) or oxidized low-density lipoprotein (oxLDL),

Cited by 13 publications

References 40 publications

Luminol-conjugated cyclodextrin biological nanoparticles for the treatment of severe burn-induced intestinal barrier disruption

Luminol-conjugated cyclodextrin biological nanoparticles for the treatment of severe burn-induced intestinal barrier disruption

Monocytic Cell Adhesion to Oxidised Ligands: Relevance to Cardiovascular Disease

Association between abnormal lipid metabolism and tumor

Contact Info

Product

Resources

About