Curcumin Reduces Tumour Necrosis Factor-Enhanced Annexin V-Positive Microparticle Release in Human Vascular Endothelial Cells

Abstract

-PURPOSE:Circulating microparticles have been highlighted as biomarkers of cardiovascular disease state and progression. The aim of this study was to evaluate the effects of curcumin on microparticle release from endothelial cells undergoing TNF-induced cell activation and apoptosis. METHODS: This study evaluated the effects of curcumin on microparticle release, cytotoxicity, apoptosis, cell adhesion molecule expression and monocyte adhesion in EAhy926 human endothelial cells. RESULTS:The results showed that the numbers of microparticles were increased by tumour necrosis factor (TNF) or the combination of TNF and cycloheximide (CHX). Curcumin attenuated microparticle release caused by TNF or TNF plus CHX treatments. The pretreatment by curcumin not only negated the accelerated cell death and apoptosis caused by TNF and CHX, but also diminished TNF-induced cell activation, as assessed by reduced surface expression of intercellular adhesion molecule 1, and adhesion of monocytes to endothelial monolayers. CONCLUSION: Curcumin reduced microparticle release from endothelial cells undergoing cell activation and apoptosis, which supports its protective role in TNF-associated endothelial dysfunction, and highlights its potential use as a nutraceutical agent for vascular inflammatory diseases.

Extracellular vesicles as mediators of immunopathology in infectious diseases

“…In a model of cytokine‐induced endothelial stimulation, curcumin was able to significantly reduced MV release. This compound not only reduced cell death and apoptosis caused by TNF, but also diminished TNF‐induced cell activation, as assessed by reduced surface expression of intercellular adhesion molecule 1, and adhesion of monocytes to endothelial monolayers . In HCV, inhibiting exosome release reduced Tfr expansion and thereby ameliorated immunosuppression .…”

Do we know enough to find an adjunctive therapy for cerebral malaria in African children?

“…This leaves two alternatives, namely studies in vitro and in animal models. Currently, there are several promising studies in vitro targeting brain endothelial activation 37 with pantethine 38 , curcumin 39 , and diannexin 40 . These experimental data have the advantage of using human brain endothelial cells and human parasites but have the shortcomings of any in vitro system.…”

Curcumin and its allied analogues: epigenetic and health perspectives - a review

“…Balanced the activity of antioxidant defense system Nariya et al (2017) Lowered the content of mtDNA and enhanced the content of Cyt B and NADH5 in spermatozoa Decreased the expression of phospho (p)-p38, p-checkpoint kinase 1 (ChK1), cyclin D1, and breast cancer associated gene 1 (BRCA1) protein; Inhibited glucose-regulated protein 78 and DNA damage Dai et al (2017) Inhibited Wnt/β-catenin signalling pathways Wang et al (2016) Restored histone deacetylase activity and used to curtail lung diseases which are unresponsive to corticosteroids Bruck et al (2007) Inhibited cytochrome P450 and UDP-glucuronosyl transferases; Lowered thioacetamide and endotoxin induced liver dysfunction via inhibiting the expression of enzymes (iNOS), transcription factors NF-кB, tumor necrosis factor-a and IL-1b Shapiro et al (2006) Lowered the ritonavir related vascular dysfunction, kidney toxicity and indomethacin-induced intestinal damage in porcine coronary arteries of rats Induced apoptotic death, reduced surface expression of intercellular adhesion molecule 1; Lowered adhesion of monocytes to endothelial monolayers Kam et al (2015) Downregulated expression of hypertrophy marker genes (ANF, β-MHC), apoptotic mediators (Bax, Cytochrome-c) and activity of apoptotic markers (Caspase 3 and PARP) Ray et al (2016) Suppressed the p300-induced hypertrophic responses and inhibits the acetylation of histones and GATA4 in cultured neonatal cardiomyocytes Balasubramanyam (2004) Mediated the suppression of nuclear acetylation; Prevented from the p300-GATA4 formation in cardiac patients Thompson (2004); Black (2006) Lowered hypertrophic responses in cardiomyocytes; Inhibited hypertrophy-responsive transcription factors; Suppressed acetylation of histones Gardner (2003) Inhibited HAT mutp300-and TSA Sano (2007) Protected from the development of atherosclerotic lesions Suppressed the IL-1β and TNF-α cytokines Bruck et al (2007) Modulated NF-κB activity Oakley et al (2005) Suppressed the hepatic fibrosis; Inhibited collagen a1 (I) gene expression & HSC activation Bruck et al (2007) Suppressed a-smooth muscle actin, collagen a1, and fibronectin (I); Increased the matrix metalloproteinase-2 and -9 expressions; Inhibited the connective tissue growth factor (CTGF) expression Xu et al (2003b) Modulated the intracellular signalling pathways i.e. JNK, PPAR-g, AP-1, ERK, and NF-κB Zheng et al (2007) Activated the PPAR-g through inhibiting NF-кB activity in HSCs Park et al (2000) Inhibited CTGF expression in HSCs; Suppressed the activation of ERK, MAP kinase and NF-κB Hsu & Cheng (2007) Antidepressant activity…”

“…Curcumin also exerts an antioxidant potential against Cd toxicity directly and/or indirectly through neutralising free radicals, metal chelating ability, increasing the antioxidant enzyme concentration, regulating inflammatory enzymes, reducing the gastrointestinal absorption and tissue Cd accumulation (Kukongviriyapan et al 2016). The earlier investigations of Kam et al (2015) illustrated the preventive role of curcumin against EAhy926 human endothelial cells through multiple mechanisms such as (1) attenuation of microparticle release caused by TNF, (2) acceleration the cell death, (3) induction of apoptotic death, and (4) reduction of the surface expression of intercellular adhesion molecule 1 and adhesion of monocytes to endothelial monolayers (Kam et al 2015).…”