Caffeic acid phenethyl ester suppresses monocyte adhesion to the endothelium by inhibiting NF-κB/NOX2-derived ROS signaling

Nakahara, Risa; Makino, Junya; Kamiya, Tetsuro; Hara, Hirokazu; Adachi, Tetsuo

doi:10.3164/jcbn.15-94

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…Dexmedetomidine Attenuated U937-HUVEC Adhesion and Adhesion of Molecule Expression in U937Monocytes via Inhibiting NOX2-Mediated ROS Production. NOX2induced ROS generation is always considered to play an important part in monocyte-endothelial adherence[21,22]. Thus, we detected the effects of dexmedetomidine (0.1 nM and 1 nM for 24 hours) on NOX2/ROS signaling pathway in the present study.Figures 2(a)and 2(b) demonstrate that LPS could activate NOX2/ROS signaling pathway in U937 monocytes, manifested as ROS production and NOX2 expression increase, while dexmedetomidine inhibited it effectively.…”

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confidence: 58%

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Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

Chai

Cao

et al. 2020

Oxidative Medicine and Cellular Longevity

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Dexmedetomidine is widely used for sedating patients in operation rooms or intensive care units. Its protective functions against oxidative stress, inflammation reaction, and apoptosis have been widely reported. In present study, we explored the effects of dexmedetomidine on monocyte-endothelial adherence. We built lipopolysaccharide- (LPS-) induced monocyte-endothelial adherence models with U937 monocytes and human umbilical vein endothelial cells (HUVECs) and observed the effects of dexmedetomidine on U937-HUVEC adhesion. Specific siRNA was designed to knock-down Connexin43 (Cx43) expression in U937 monocytes. Gö6976, GSK2795039, and NAC were used to inhibit PKC-α, NOX2, and ROS, respectively. Then, we detected whether dexmedetomidine could downregulate Cx43 expression and its downstream PKC-α/NOX2/ROS signaling pathway activation and ultimately result in the decrease of U937-HUVEC adhesion. The results showed that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), could inhibit adhesion of molecule expression (VLA-4 and LFA-1) and U937-HUVEC adhesion. Simultaneously, it also attenuated Cx43 expression in U937 monocytes. With the downregulation of Cx43 expression, the activity of PKC-α and its related NOX2/ROS signaling pathway were reduced. Inhibiting PKC-α/NOX2/ROS signaling pathway with Gö6976, GSK2795039, and NAC, respectively, VLA-4, LFA-1 expression, and U937-HUVEC adhesion were all decreased. In summary, we concluded that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), decreased Cx43 expression in U937 monocytes and PKC-α associated with carboxyl-terminal domain of Cx43 protein. With the downregulation of PKC-α, the NOX2/ROS signaling pathway was inhibited, resulting in the decrease of VLA-4 and LFA-1 expression. Ultimately, U937-HUVEC adhesion was reduced.

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confidence: 58%

“…NOX2-induced ROS generation is always considered to play an important part in monocyte-endothelial adherence [ 21 , 22 ]. Thus, we detected the effects of dexmedetomidine (0.1 nM and 1 nM for 24 hours) on NOX2/ROS signaling pathway in the present study.…”

Section: Resultsmentioning

confidence: 99%

Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

Chai

Cao

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…( 8 , 36 ) We recently reported that a treatment with CAPE suppressed monocyte adhesion to endothelial cells by inhibiting the accumulation of intracellular ROS. ( 37 ) In this study, we determined that pretreatment with CAPE significantly suppressed H 2 O 2 or 6-OHDA-triggered HREC cell injury (Fig. 1 B).…”

Section: Discussionmentioning

confidence: 73%

CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells

Ohashi

Yasuda

Kamiya

et al. 2017

J. Clin. Biochem. Nutr.

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Extracellular-superoxide dismutase (EC-SOD or SOD3), which catalyzes the dismutation of superoxide anions into hydrogen peroxide, plays a key role in vascular protection against reactive oxygen species (ROS). The excess generation of ROS is closely involved in the pathogenesis of diabetic retinopathy (DR); therefore, the maintenance of SOD3 expression at high levels is important for the prevention of DR. In the present study, we showed that caffeic acid phenethyl ester (CAPE) increased the expression of SOD3 through the acetylation of histone within the SOD3 promoter region in human retinal endothelial cells (HRECs). Histone acetylation within its promoter was focused on the inhibition of histone deacetylase (HDAC), and we examined the involvement of myocyte enhancer factor 2 (MEF2) and HDAC1 in CAPE-elicited SOD3 expression. Our results demonstrate that SOD3 silencing in basal HRECs is regulated by HDAC1 composed with MEF2A/2D hetero dimers. Moreover, phosphorylation of threonine 312 in MEF2A and dissociation of HDAC1 from SOD3 promoter play pivotal roles in CAPE-elicited SOD3 expression. Overall, our findings provide that CAPE may be one of the seed compounds that maintain redox homeostasis.

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“…The adhesion of monocytes to the endothelium, followed by their infiltration and differentiation into macrophages, determines the initiation and progression of atherosclerosis (Liu et al., ). Previous studies have established that pretreated HUVECs with other polyphenolic compounds, such as caffeic acid phenethyl ester and epigallocatechin gallate (EGCG), could reduce monocytes adhesion to endothelial cells HUVECs (Li et al., ; Nakahara, Makino, Kamiya, Hara, & Adachi, ; Yamagata, Tagami, & Yamori, ). In the present study, we found that the control group showed minimal binding to U937 cells, whereas HUVECs showed more attractive to monocytes after IL‐1β treatment.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have established that pretreated HUVECs with other polyphenolic compounds, such as caffeic acid phenethyl ester and epigallocatechin gallate (EGCG), could reduce monocytes adhesion to endothelial cells HUVECs (Li et al, 2012;Nakahara, Makino, Kamiya, Hara, & Adachi, 2016;Yamagata, Tagami, & Yamori, 2015).…”

Section: Discussionmentioning

confidence: 99%

Curcumin suppresses pro-inflammatory adhesion response in Human Umbilical Vein Endothelial Cells

Chang

Cheng

2018

J Food Biochem

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Atherosclerosis, a progressive pathological disorder, is a leading cause of human morbidity and mortality worldwide. The expression of cell adhesion molecules by the endothelium and the attachment of monocytes to endothelium may play a pivotal role in the early atherogenic process. Curcumin, a polyphenol obtained from the root of turmeric, is the main component of curry powder. Previous studies indicated that curcumin exhibits a variety of pharmacological effects, including anti‐inflammatory, antitumor, antioxidant, and anti‐hypertensive properties. In the current study, we found that curcumin could suppress the IL‐1β‐induced intracellular reactive oxygen species production and the activation of redox‐sensitive transcription factors NF‐κB p50 and p65. Moreover, curcumin could inhibit the expression of adhesion molecules, including intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), and E‐selectin, and further decrease the adhesiveness to a human monocytic cell line (U937) in human umbilical vein endothelial cells (HUVECs). These findings may identify the novel role and potential translational application of curcumin, suggesting its potential applicability as an anti‐atherosclerotic agent. Practical applications In the current study, we examine the inhibitory effects of curcumin on monocyte adhesion to cultured human endothelial cells and the expression of adhesion molecules by IL‐1β in HUVECs and elucidate its possible mechanism of action. Our findings may identify the novel role and potential translational application of curcumin, suggesting its potential applicability as an anti‐atherosclerotic agent.

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Caffeic acid phenethyl ester suppresses monocyte adhesion to the endothelium by inhibiting NF-κB/NOX2-derived ROS signaling

Cited by 6 publications

References 42 publications

Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

CAPE increases the expression of SOD3 through epigenetics in human retinal endothelial cells

Curcumin suppresses pro-inflammatory adhesion response in Human Umbilical Vein Endothelial Cells

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