Stereoselective suppressive effects of protopanaxadiol epimers on UV-B-induced reactive oxygen species and matrix metalloproteinase-2 in human dermal keratinocytes

2015 ◽  
Vol 93 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Sun-Joo Oh ◽  
Sihyeong Lee ◽  
Ye Eun Kho ◽  
Kyunghoon Kim ◽  
Chang Duck Jin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Western Blot ◽  
Conditioned Medium ◽  
Reactive Oxygen ◽  
Gelatin Zymography ◽  
Human Keratinocytes ◽  
Inhibitory Effect ◽  
Matrix Metalloproteinase 2 ◽  
Hacat Cells ◽  
Oxygen Species

This study aimed to assess the skin-related anti-photoaging activities of the 2 epimeric forms of protopanaxadiol (PPD), 20(S)-PPD and 20(R)-PPD, in cultured human keratinocytes (HaCaT cells). The anti-photoaging activity was evaluated by analyzing the levels of reactive oxygen species (ROS) and matrix metalloproteinases (MMPs), as well as cell viability for HaCaT cells under UV-B irradiation. The activities for MMP-2 and -1 in conditioned medium were determined using gelatin zymography, and MMP-2 protein in the conditioned medium was detected using Western blot analysis. 20(S)-PPD, but not 20(R)-PPD, suppressed UV-B-induced ROS elevation. Neither of the epimers, at the concentrations used, exhibited cytotoxicity, irrespective of UV-B irradiation. 20(S)-PPD, but not 20(R)-PPD, exhibited an inhibitory effect on UV-B-induced MMP-2 activity and expression in HaCaT cells. In brief, only 20(S)-PPD, a major metabolic product of PPD-type ginsenosides, inhibits UV-B-induced ROS and MMP-2 elevation, implying its stereospecific anti-photoaging activity on the skin.

scholarly journals Protective effect of kudzu root vinegar and adenosine against UVB-induced oxidative stress in human keratinocytes

2020 ◽  
Vol 3 (2) ◽  
pp. 184-192
Author(s):  
Ji Eun Park ◽  
◽  
Young Mi Kim
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hacat Cell ◽  
Reactive Oxygen ◽  
Human Keratinocytes ◽  
Mitogen Activated Protein Kinase ◽  
Hacat Cells ◽  
Oxygen Species ◽  
Protective Effects ◽  
Skin Damage

Ultraviolet (UV) irradiation generates reactive oxygen species (ROS) in cells, which induces sunburn cell formation, melanoma, photoaging, and skin cancer. This study examines the anti-photodamage effects of kudzu root vinegar and adenosine in UVB-exposed human keratinocytes (HaCaT cells). UVB significantly decreased HaCaT cell viability, whereas kudzu root vinegar and adenosine did not exhibit cytotoxic effects and increased the viability of HaCaT cells. To investigate the protective effects of kudzu root vinegar and adenosine on UVB-induced oxidative stress in HaCaT cells, ROS, matrix metalloproteinases (MMPs), and mitogen-activated protein kinase (MAPK) were analyzed. UVB-induced treatment reduced the activity of antioxidant enzymes; however, kudzu root vinegar and adenosine increased their activity. These results indicated that kudzu root vinegar and adenosine exert cytoprotective activity against UVB-induced oxidative stress in HaCaT cells. Moreover, they suppressed the UVB-induced downregulation of MMPs and inhibited the phosphorylation of MAPK induced by UVB-irradiation. Therefore, kudzu root vinegar and adenosine offer anti-oxidative effects, via lowering ROS production, suppressing JNK activation, and downregulating expression of MMPs. Our findings suggest that kudzu root vinegar and adenosine have potential application in preventing skin damage owing to UVB exposure. Keywords: reactive oxygen species (ROS), HaCaT cell, UVB, skin damage, anti-aging

Adipose stromal cells-conditioned medium blocks 6-hydroxydopamine-induced neurotoxicity and reactive oxygen species

2013 ◽  
Vol 544 ◽  
pp. 15-19 ◽  
Author(s):  
Huiying Gu ◽  
Jimmy Wang ◽  
Nicole Du ◽  
Jiangning Tan ◽  
Brian Johnstone ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Conditioned Medium ◽  
Stromal Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Adipose Stromal Cells ◽  
6 Hydroxydopamine

scholarly journals Reactive Oxygen Species-Mediated Cezanne Inactivation by Oxidation of its Catalytic Cysteine Residue in Hepatocellular Carcinoma

2019 ◽  
Vol 27 (9) ◽  
pp. 1069-1077
Author(s):  
Zhongyuan Yin ◽  
Lin Yang ◽  
Feng Wu ◽  
Jinshuo Fan ◽  
Juanjuan Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Matrix Metalloproteinase 2 ◽  
Intercellular Adhesion Molecule ◽  
Oxygen Species ◽  
Cysteine Oxidation ◽  
Diphenylene Iodonium ◽  
Hcc Cells ◽  
Inflammatory Effect

Cysteine oxidation occurs at the active site of deubiquitinases (DUBs) during many biologic signaling cascades. Here we report that hepatocellular carcinoma cells (HCCs) generated higher levels of endogenous reactive oxygen species (ROS). This elevated ROS production was inhibited by NADPH oxidase inhibitor diphenylene iodonium (DPI) and mitochondria electron chain inhibitor rotenone in HCC cells. Moreover, we found that H2O2 could activate NF-κB-dependent inflammatory effect through increased induction of matrix metalloproteinase 2 (MMP2), MMP9, and intercellular adhesion molecule 1 (ICAM1) expression levels. In addition, we found that H2O2 could prolong NF-κB activation by suppressing the negative regulatory functions of Cezanne in HCC cells. Ubiquitin-derived thiol-reactive probe (HA-UbVME) assay and biotin-tagged 1,3-cyclohexadione derivative (DCP-Bio1) assay showed that H2O2 has the capacity to inhibit the catalytic activity of Cezanne, and the reducing agent, DTT, could reactivate the Cezanne deubiquitinating enzyme activity. Taken all together, these findings demonstrated an important role for oxidation of Cezanne by ROS in regulation of the inflammatory effect of hepatocellular carcinoma.

scholarly journals Modulation of metabolic activity of phagocytes by antihistamines

2011 ◽  
Vol 4 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Antonin Lojek ◽  
Milan Číž ◽  
Michaela Pekarová ◽  
Gabriela Ambrožová ◽  
Ondřej Vašíček ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Metabolic Activity ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Inhibitory Effect ◽  
Oxygen Species ◽  
Antioxidative Properties ◽  
Enhanced Chemiluminescence ◽  
Inos Protein Expression

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.

scholarly journals 3-Bromopyruvate potentiates TRAIL-induced apoptosis in human colon cancer cells through a reactive oxygen species- and caspase-dependent mitochondrial pathway

2019 ◽  
Vol 97 (12) ◽  
pp. 1176-1184 ◽  
Author(s):  
Hassan Abbaszadeh ◽  
Armita Valizadeh ◽  
Masoud Mahdavinia ◽  
Ali Teimoori ◽  
Mohammad Hassan Pipelzadeh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Reactive Oxygen ◽  
Human Colon ◽  
Inhibitory Effect ◽  
Oxygen Species ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Normal Cells

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.

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