Phytoglycoprotein (75 kDa) inhibits expression of interleukin‐1β stimulated by DEHP in human mast cells

Abstract

The purpose of this study is to investigate the inhibitory effect of a glycoprotein (CTB glycoprotein, 75 kDa) isolated from Cudrania tricuspidata Bureau (CTB) on the di-(2-ethylhexyl)phthalate (DEHP) induced expression of allergic-inflammation-related mediators in human mast cells. The changes on the levels of intracellular reactive oxygen species (ROS), mitogen-activated protein kinase (MAPK), transcription factor [nuclear factor (NF)-kappaB], and allergic inflammatory mediators [cyclooxygenase (COX)-2 and interleukin (IL)-1beta] were evaluated using Western blot and RT-PCR. Our results showed that the CTB glycoprotein in the presence of DEHP inhibits the production of intracellular ROS, the phosphorylation of ERK1/2, and p38 MAPK in HMC-1 cells. In addition, the CTB glycoprotein has suppressive effects on the transcriptional activation of NF-kappaB, and on the expression levels of COX-2 and IL-1beta in DEHP-treated HMC-1 cells. In conclusion, the CTB glycoprotein has a strong anti-inflammatory effect on the activities of allergic inflammatory mediators indirectly caused by DEHP in HMC-1 cells.

ICAM-1 and IL-8 Are Expressed by DEHP and Suppressed by Curcumin Through ERK and p38 MAPK in Human Umbilical Vein Endothelial Cells

“…Our results revealed that pretreatment with MEK1 inhibitor PD98059 (20 μM) or p38 inhibitor SB203580 (25 μM) significantly reduced DEHPinduced expression of ICAM-1 and IL-8, indicating that DEHP induction of ICAM-1 and IL-8 expression was mediated through ERK1/2 and p38 signaling pathways. We also found that the relative levels of phosphorylated ERK1/2 and p38 protein were significantly upregulated following DEHP treatment for as early as 15 min, which was consistent with previous findings [7]. This induction was effectively inhibited by pretreatment of curcumin and PD98059 which suggested that the anti-inflamma- tory activity of curcumin was related to the modulation of ERK1/2 and p38 MAPK activation in HUVECs.…”

“…Increased indoor level of DEHP has been associated with an increased risk of admissions for allergic asthma and other airway diseases in children [5]. Studies have shown that DEHP has an adjuvant effect on allergen-induced immunoglobulin production through enhancing allergic-related inflammatory response including stimulation of the production of inflammatory mediators (IL-4, COX-2, TNF-alpha, and IL-8) in a variety of cell lines and in mice [6][7][8].…”

Apigenin Inhibits the Expression of IL-6, IL-8, and ICAM-1 in DEHP-Stimulated Human Umbilical Vein Endothelial Cells and In Vivo

“…In the present study, we demonstrated for the first time that apigenin flavonoid effectively attenuated DEHP-induced allergic inflammation by reduction of the expression of pro-inflammatory There were reports suggesting that phthalates including DEHP may adversely affect human immune functions, thereby enhancing the progress of allergic inflammatory disorders such as allergic asthma [23,24]. One possible reason is that phthalates have the potential to increase the expression of cytokines or chemokines in inflammatory cells [25]. DEHP was reported to cause an increase in the amount of IgG, which is associated with the development of allergic respiratory diseases [26].…”

The adjuvant effect induced by di-(2-ethylhexyl) phthalate (DEHP) is mediated through oxidative stress in a mouse model of asthma

“…A series of events related to the airway inflammation then took place, and vice versa (Nose, 2000;Manojkumar et al, 1998). Specifically, the intracellular GSH level in antigen-presenting cells influenced the Th1/Th2 cytokine response pattern, and more precisely, GSH depletion inhibited the Th1-associated cytokine production and/or favored the Th2 associated responses (Oh et al, 2010). Meanwhile, the increased MDA level in lung tissue could enhance the leucocyte chemotaxis and alter histamine release, thus perpetuating inflammation.…”