Inhibitory effect of caffeic acid phenethyl on adipocyte differentiation through regulation of reactive oxygen species in the 3T3-L1 cell model

2018 ◽  
Vol 120 ◽  
pp. S48-S49
Author(s):  
DaeKun Lee
Author(s):  
Dumitriţa RUGINǍ ◽  
Adela PINTEA ◽  
Raluca PÂRLOG ◽  
Andreea VARGA

Oxidative stress causes biological changes responsible for carcinogenesis and aging in human cells. The retinal pigmented epithelium is continuously exposed to oxidative stress. Therefore reactive oxygen species (ROS) and products of lipid peroxidation accumulate in RPE. Neutralization of ROS occurs in retina by the action of antioxidant defence systems. In the present study, the protective effect of caffeic acid (3,4-dihydroxy cinnamic acid), a dietary phenolic compound, has been examined in normal and in oxidative stress conditions (500 µM peroxide oxygen) in cultures human epithelial pigment retinal cells (Nowak, M. et al.). The cell viability, the antioxidant enzymes activity (CAT, GPx, SOD) and the level of intracellular reactive oxygen species (ROS) were determined. Exposure to l00 µM caffeic acid for 24 h induced cellular changes indicating the protective effect of caffeic acid in RPE cells. Caffeic acid did not show any cytotoxic effect at concentrations lower than 200 μM in culture medium. Treatment of RPE cells with caffeic acid causes an increase of catalase, glutathione peroxidase and superoxide dismutase activity, especially in cells treated with hydrogen peroxide. Caffeic acid causes a decrease of ROS level in cells treated with hydrogen peroxide. This study proved that caffeic acid or food that contain high levels of this phenolic acid may have beneficial effects in prevention of retinal diseases associated with oxidative stress by improving antioxidant defence systems.


2011 ◽  
Vol 4 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Antonin Lojek ◽  
Milan Číž ◽  
Michaela Pekarová ◽  
Gabriela Ambrožová ◽  
Ondřej Vašíček ◽  
...  

Modulation of metabolic activity of phagocytes by antihistaminesThe purpose of the study was to investigate the effects of H1-antihistamines of the 1stgeneration (antazoline, bromadryl, brompheniramine, dithiaden, cyclizine, chlorcyclizine, chlorpheniramine, clemastine) and the 2ndgeneration (acrivastine, ketotifen, and loratadine) on the respiratory burst of phagocytes. Reactive oxygen species generation in neutrophils isolated from rat blood was measured using luminol-enhanced chemiluminescence. Changes in nitrite formation and iNOS protein expression by RAW 264.7 macrophages were analysed using Griess reaction and Western blotting. The antioxidative properties of drugs in cell-free systems were detected spectrophotometrically, luminometrically, fluorimetrically, and amperometrically. The majority of the H1-antihistamines tested (bromadryl, brompheniramine, chlorcyclizine, chlorpheniramine, clemastine, dithiaden, and ketotifen) exhibited a significant inhibitory effect on the chemiluminescence activity of phagocytes. H1-antihistamines did not show significant scavenging properties against superoxide anion and hydroxyl radical, thus this could not contribute to the inhibition of chemiluminescence. H1-antihistamines had a different ability to modulate nitric oxide production by LPS-stimulated macrophages. Bromadryl, clemastine, and dithiaden were the most effective since they inhibited iNOS expression, which was followed by a significant reduction in nitrite levels. H1-antihistamines had no scavenging activity against nitric oxide. It can be concluded that the effects observed in the H1-antihistamines tested are not mediated exclusively via H1-receptor pathway or by direct antioxidative properties. Based on our results, antihistamines not interfering with the microbicidal mechanisms of leukocytes (antazoline, acrivastine and cyclizine) could be used preferentially in infections. Other antihistamines should be used, under pathological conditions accompanied by the overproduction of reactive oxygen species.


2009 ◽  
Vol 284 (16) ◽  
pp. 10601-10609 ◽  
Author(s):  
Haemi Lee ◽  
Yoo Jeong Lee ◽  
Hyeonjin Choi ◽  
Eun Hee Ko ◽  
Jae-woo Kim

2018 ◽  
Vol 12 (20) ◽  
pp. 263-268 ◽  
Author(s):  
Brito Dantas Mariana ◽  
Lima Sampaio Tiago ◽  
Róseo Paula Pessoa Bezerra de Menezes Ramon ◽  
Magalhães Ferreira Jamile ◽  
Sousa Melo Tiago ◽  
...  

2019 ◽  
Vol 97 (12) ◽  
pp. 1176-1184 ◽  
Author(s):  
Hassan Abbaszadeh ◽  
Armita Valizadeh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
Mohammad Hassan Pipelzadeh ◽  
...  

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a promising anticancer cytokine with minimal toxicity towards normal cells. Nevertheless, most primary cancers are often intrinsically TRAIL-resistant or can acquire resistance after TRAIL therapy. This study aimed to investigate the inhibitory effect of co-treatment of 3-bromopyruvate (3-BP) as a potent anticancer agent with TRAIL on colon cancer cells (HT-29). The results of present study indicated that combined treatment with 3-BP and TRAIL inhibited the proliferation of HT-29 cells to a greater extent (88.4%) compared with 3-BP (54%) or TRAIL (11%) treatment alone. In contrast, the combination of 3-BP and TRAIL had no significant inhibitory effect on the proliferation of normal cells (HEK-293) (8.4%). At a cellular mechanistic level, the present study showed that 3-BP sensitized human colon cancer cells to TRAIL-induced apoptosis via reactive oxygen species generation, upregulation of Bax, downregulation of Bcl-2 and survivin, release of cytochrome c into the cytosol, and activation of caspase-3. In normal cells, 3-BP, TRAIL, or combination of both had no significant effect on the reactive oxygen species levels, release of cytochrome c, and caspase-3 activity. Therefore, the combination of 3-BP and TRAIL can be a promising therapeutic strategy for treatment of colon cancer.


2003 ◽  
Vol 96 (1) ◽  
pp. 89-91 ◽  
Author(s):  
Akiko Murata ◽  
Keizo Sekiya ◽  
Yasuo Watanabe ◽  
Fuminori Yamaguchi ◽  
Naoya Hatano ◽  
...  

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