scholarly journals Identification of Pathways and Key Genes in Carotid Atherosclerosis by Bioinformatics Analysis

2021 ◽  
Author(s):  
Di Zhang ◽  
Bei Jing ◽  
Xin Li ◽  
Huimei Shi ◽  
Shiquan Chang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Palmitic Acid ◽  
Experimental Verification ◽  
Carotid Atherosclerosis ◽  
Mrna Level ◽  
Reactive Oxygen ◽  
Control Group ◽  
Mrna Levels ◽  
Oxygen Species ◽  
Huvec Cells

Abstract Purpose: Carotid atherosclerosis is a serious vascular disease, leading to various cerebrovascular diseases. Methods: Gene expression profile of GSE100927 was selected to conduct differentially expressed genes. Then we performed protein-protein interactions, Gene ontology, and Kyoto Encyclopedia of Genes and Genomes analysis. Then we used HUVEC, HAVSMC, and THP-1 induced macrophages cells to conduct experimental verification. The experimental groups were as follows: Control group, Solvent control group, and Palmitic acid group. We measured the levels of reactive oxygen species in three cells via flow cytometer or fluorescence microscope. Then we detected apoptosis of HUVEC cells and HAVSMC cells or observed nucleus of THP-1 induced macrophages cells. Results: We selected male carotid atherosclerosis, with 10 control samples and 21 atherosclerosis samples. The results of pathway enrichment showed that “Toll-like receptor signaling pathway” ranked first. We chose IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 for experimental verification. Palmitic acid increased the reactive oxygen species levels and the apoptosis rates of HUVEC cells and HAVSMC cells while increasing the activity of THP-1 induced macrophages cells, and it cannot increase the level of reactive oxygen species, and shrink the nucleus. Palmitic acid increased mRNA levels of IL1β, CCL4, SPP1, CCL3, IRF5. MMP7 and MMP9 in HUVEC cells and THP-1 induced macrophages, and increased the mRNA levels of CCL4 and MMP9 in HAVSMC cells，not changed the mRNA level of IRF5. Conclusion: IL1β，CCL3, CCL4, SPP1, IRF5, MMP7, and MMP9 are significant markers of carotid atherosclerosis.

scholarly journals Qizhi Jiangtang Jiaonang Improves Insulin Signaling and Reduces Inflammatory Cytokine Secretion and Reactive Oxygen Species Formation in Insulin Resistant HepG2 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8
Author(s):  
Xiao-Tian Zhang ◽  
Chun-Jiang Yu ◽  
Jian-Wei Liu ◽  
Yan-Ping Zhang ◽  
Chao Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Palmitic Acid ◽  
Hepg2 Cells ◽  
Reactive Oxygen ◽  
Glucose Consumption ◽  
Control Group ◽  
High Dose ◽  
Oxygen Species ◽  
Insulin Resistant

We analyzed the effects of a traditional Chinese medicine, Qizhi Jiangtang Jiaonang (QJJ), on insulin resistance (IR) in vitro. After an in vitro model of IR was established by treating human liver cancer cells (HepG2 cells) with palmitic acid, the cells were then treated with various concentrations of QJJ. Treatment with 400 µM palmitic acid for 24 h induced IR in HepG2 cells. The survival rate for HepG2 cells in the IR group was significantly lower than that of the untreated control group (P< 0.001); however, QJJ restored HepG2 cell survival (P< 0.001). As compared with HepG2 cells in the IR group, QJJ at all doses analyzed significantly increased glucose consumption (allP< 0.05). Moreover, treatment with all the QJJ doses significantly reduced the mean intracellular reactive oxygen species levels as compared with the IR group (allP< 0.05). Furthermore, high-dose QJJ reduced both TNF-αand IL-6 levels as compared to the IR group (allP< 0.05). QJJ ameliorated the altered PI3K, GLUT4, and RAGE expression observed with IR. In conclusion, QJJ can improve IR in HepG2 cells, which may be mediated through the IRS-1/PI3K/GLUT4 signaling pathway as well as regulation of NF-κB-mediated inflammation and oxidative stress.

scholarly journals SPARC Levels Modulate the Capacity of Mitomycin to Inhibit the Proliferation of Human Tenon’s Capsule Fibroblasts

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Yuanyuan Guo ◽  
Shouxiang Ni ◽  
Weiyan Zhou ◽  
Jiangping Hou ◽  
Jiaquan Shen
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Density ◽  
Collagen Gel ◽  
Reactive Oxygen ◽  
Control Group ◽  
Mrna Levels ◽  
Oxygen Species ◽  
Antifibrotic Effect ◽  
Cell Densities

Purpose. To evaluate the role of SPARC in the antiproliferation effect of MMC on human Tenon’s fibroblasts (HTF). Method. Sixteen PACG patients aged 59 ± 10 years (31–72 years), including 6 males and 10 females, were recruited. Tenon tissue was harvested during filtering surgery. Cell density was evaluated after MMC application with different concentrations and application times, by which the optimized MMC application modality was determined. MMC, si-SPARC, or SPARC protein was used when needed to evaluate the cell densities under different conditions, by which the role of SPARC in MMC-mediated antifibrotic process was identified. Results. Considering that the cell densities, as well as SPARC expression on mRNA and protein levels, are relatively stable when the MMC concentration is higher than 0.02% and exposure time longer than 90 s, we chose the MMC application pattern with 0.02% and 90 s as an optimized pattern for the downstream work. Compared to control, the si-SPARC and MMC downregulated the SPARC protein by 91% (P<0.01) and 65% (P<0.01) and mRNA by 96% (P<0.01) and 64% (P<0.01), respectively. MMC decreases the cell densities by 53.50% compared to control. si-SPARC + MMC dramatically deceased the cell density no matter compared to the control group (P<0.01) or MMC group (P<0.01); correspondingly, the relative collagen gel area in the MMC + si-SPARC group was higher than that in the MMC group or si-SPARC group (P<0.05). The reactive oxygen species expression in the MMC + si-SPARC group is higher than that in the MMC group (P<0.05). Conclusion. This study demonstrates that in HTF, (1) MMC downregulates the expression of SPARC in protein and mRNA levels; (2) SPARC depletion has synergistic effect on the antifibrotic effect of MMC; and (3) reactive oxygen species are the possible mediator in the antifibrotic effect of MMC and si-SPARC.

Altered composition of high-lipid diet may generate reactive oxygen species by disturbing the balance of antioxidant and free radicals

2020 ◽  
Vol 31 (3) ◽  
Author(s):  
Arnab Banerjee ◽  
Debasmita Das ◽  
Rajarshi Paul ◽  
Sandipan Roy ◽  
Ankita Bhattacharjee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Reactive Oxygen ◽  
Control Group ◽  
Preliminary Evaluation ◽  
Oxygen Species ◽  
High Lipid ◽  
Tnf Α ◽  
High Lipid Diet ◽  
Lipid Diet

AbstractBackgroundIn the present era, obesity is increasing rapidly, and high dietary intake of lipid could be a noteworthy risk factor for the occasion of obesity, as well as nonalcoholic fatty liver disease, which is the independent risk factor for type 2 diabetes and cardiovascular disease. For a long time, high-lipid diet (HLD) in “fast food” is turning into part of our everyday life. So, we were interested in fulfilling the paucity of studies by means of preliminary evaluation of these three alternative doses of HLD on a rat model and elucidating the possible mechanism of these effects and divulging the most alarming dose.MethodsThirty-two rats were taken, and of these, 24 were fed with HLD in three distinctive compositions of edible coconut oil and vanaspati ghee in a ratio of 2:3, 3:2 and 1:1 (n = 8), orally through gavage at a dose of 10 mL/kg body weight for a period of 28 days, whereas the other eight were selected to comprise the control group.ResultsAfter completion of the experiment, followed by analysis of data it was revealed that hyperlipidemia with increased liver and cardiac marker enzymes, are associated with hepatocellular injury and cardiac damage. The data also supported increased proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). As oxidative stress parameter increased in both liver and heart, there is also an increased in TNF-α due to an increased expression of inducible nitric oxide (NO) synthase, which led to a high production of NO. Moreover, HLD treatment explicitly weakens reasonability of hepatocytes and cardiomyocytes conceivably through G0/G1 or S stage capture or perhaps by means of enlistment of sub-G0/G1 DNA fragmentation and a sign of apoptosis.ConclusionsBased on the outcomes, it tends to be inferred that consequences of the present examination uncovered HLD in combination of 2:3 applies most encouraging systemic damage by reactive oxygen species generation and hyperlipidemia and necroapoptosis of the liver and heart. Hence, outcome of this study may help to formulate health care strategy and warns about the food habit in universal population regarding the use of hydrogenated and saturated fats (vanaspati ghee) in diet.

Reactive oxygen species modulate HIF-1 mediated PAI-1 expression: involvement of the GTPase Rac1

2003 ◽  
Vol 89 (05) ◽  
pp. 926-935 ◽  
Author(s):  
Utta Berchner-Pfannschmidt ◽  
Christoph Wotzlaw ◽  
Robbert Cool ◽  
Joachim Fandrey ◽  
Helmut Acker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Plasminogen Activator Inhibitor ◽  
Dominant Negative ◽  
Mrna Levels ◽  
Ros Production ◽  
Oxygen Species ◽  
Plasminogen Activator Inhibitor 1 ◽  
Pai 1

SummaryThe hypoxia-inducible transcription factor HIF-1 mediates upregulation of plasminogen activator inhibitor-1 (PAI-1) expression under hypoxia. Reactive oxygen species (ROS) have also been implicated in PAI-1 gene expression. However, the role of ROS in HIF-1-mediated regulation of PAI-1 is not clear. We therefore investigated the role of the GTPase Rac1 which modulates ROS production in the pathway leading to HIF-1 and PAI-1 induction.Overexpression of constitutively activated (RacG12V) or dominant-negative (RacT17N) Rac1 increased or decreased, respectively, ROS production. In RacG12V-expressing cells, PAI-1 mRNA levels as well as HIF-1α nuclear presence were reduced under normoxia and hypoxia whereas expression of RacT17N resulted in opposite effects. Treatment with the antioxidant pyrrolidinedithiocarbamate or coexpression of the redox factor-1 restored HIF-1 and PAI-1 promoter activity in RacG12V-cells. In contrast, NFκB activation was enhanced in RacG12V-cells, but abolished by RacT17N. Thus, these findings suggest a mechanism explaining modified fibrinolysis and tissue remodeling in an oxidized environment.

scholarly journals Decrease in generation of reactive oxygen species by neutrophils from patients with infectious mononucleosis: role of suppressor T lymphocytes

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 994-999
Author(s):  
Y Niwa ◽  
T Sakane ◽  
Y Miyachi ◽  
T Kanoh ◽  
K Somiya
Keyword(s):  
Reactive Oxygen Species ◽  
T Lymphocytes ◽  
Infectious Mononucleosis ◽  
Disease Onset ◽  
Reactive Oxygen ◽  
Control Group ◽  
Ros Generation ◽  
Oxygen Species ◽  
Suppressor T Lymphocytes ◽  
Subsets Of T Lymphocytes

We assessed the generation of reactive oxygen species (ROS: O2-, H2O2, OH . , chemiluminescence) by neutrophils and monocytes from six patients with infectious mononucleosis, ten patients with other viral diseases, and ten normal controls. Neutrophils from infectious mononucleosis patients showed markedly decreased generation of all reactive oxygen species, compared with the two control groups; this abnormality persisted for four to eight weeks after disease onset. Monocytes from these patients generated normal levels of ROS. Normal neutrophils incubated with T lymphocytes from infectious mononucleosis patients generated significantly less of each ROS than did those incubated with T cells from either control group. T cell-mediated suppression of ROS generation required both OKT4+ cells from infectious mononucleosis patients and OKT8+ cells from either patients or normals. We conclude that the generation of reaction oxygen species in neutrophils is suppressed in patients with infectious mononucleosis, at least in part, by interacting subsets of T lymphocytes.

scholarly journals High glucose promotes apoptosis and autophagy of MC3T3-E1 osteoblasts

2020 ◽  
Author(s):  
Pei Zhang ◽  
Jing Liao ◽  
Xiaoju Wang ◽  
Zhengping Feng
Keyword(s):  
Reactive Oxygen Species ◽  
High Glucose ◽  
Mitochondrial Membrane ◽  
Metabolic Diseases ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Control Group ◽  
Oxygen Species ◽  
Glucose Fluctuation ◽  
High Glucose Group

IntroductionDiabetes and osteoporosis are common metabolic diseases. Abnormal high glucose can lead to the apoptosis of osteoblasts. Autophagy is a highly conserved cellular process that degrades proteins or organelles. In the present study, we comparatively analyzed the effects of high glucose and glucose fluctuation on apoptosis and autophagy of MC3T3-E1 osteoblasts.Material and methodsMC3T3-E1 cells were respectively treated with different concentrations of D-glucose: 5.5 mM for the control group, 25 mM for the high glucose group and 5.5/25 mM for the glucose fluctuation group.ResultsHigh glucose and glucose fluctuation decreased MC3T3-E1 proliferation and activated autophagy. Also, high glucose and glucose fluctuation might induce the production of reactive oxygen species, decline the mitochondrial membrane potential and trigger apoptosis. The differences in the glucose fluctuation treatment group were more significant. Moreover, N-acetylcysteine, an antioxidant reagent, dramatically eliminated the intracellular reactive oxygen species induced by high glucose and glucose fluctuation, and significantly inhibited the autophagy and apoptosis in MC3T3-E1 osteoblasts. Furthermore, treatment with chloroquine, an inhibitor of autophagy, significantly increased the apoptosis of MC3T3-E1 osteoblasts.ConclusionsHigh glucose, especially high glucose fluctuation, inhibits proliferation and promotes apoptosis and autophagy of MC3T3-E1 osteoblasts. This may occur through inducing oxidative stress and mitochondrial damage in the osteoblasts.

A Study of Role of Reactive Oxygen Species in Idiopathic Male Infertility & Its Management by Antioxidant Therapy in Uttar Pradesh (U.P.)

2021 ◽  
Vol 8 (32) ◽  
pp. 3023-3027
Author(s):  
Namrata Shrivastava ◽  
Vaibhav Shrivastava ◽  
Manish Pandey
Keyword(s):  
Reactive Oxygen Species ◽  
Male Infertility ◽  
Reactive Oxygen ◽  
Antioxidant Therapy ◽  
Semen Parameters ◽  
Control Group ◽  
P Value ◽  
Ros Generation ◽  
Variable Degree ◽  
Oxygen Species

BACKGROUND Infertility is defined as the inability to conceive after at 1 year of regular unprotected intercourse. Male contributes to almost half of infertility cases and in almost 30 % of cases, no definite aetiology is identified, and hence, male infertility is labelled idiopathic in these cases. Oxidative energy production mechanisms are almost always accompanied by reactive oxygen species (ROS), generation whose too much concentrations can lead to extensive protein damage and cytoskeletal modifications and inhibit cellular mechanisms. A number of laboratory techniques have been developed to evaluate oxidative stress by measuring ROS level in the semen. In recent times antioxidant supplements have been proposed as useful agents to increase the scavenging capacity of seminal plasma, controversy still surrounds their actual clinical utility. METHODS 34 male patients were included in this study. Reactive oxygen species detection was done by Flowcytometry using dichloroflurosecindiacetate (DCFH-DA). RESULTS The ROS in the patient group was found to be significantly higher 29.821 (5.6300 than the control group 22.162 (1.6331 having p value < 0.001). The ROS (29.821 ± 5.6300) was found to be significantly reduced after 3 months of antioxidant therapy which got reduced to 19.893 ± 4.2299 respectively. CONCLUSIONS Our study demonstrates that infertile men have significantly higher level of ROS (as measured by flowcytometry) & lower sperm count (oligospermia), decreased progressive & total motility and increased immotile sperms as compared to healthy fertile men. This study further proves that antioxidant therapy based on a combination of carnitine, zinc, coq10, lycopene and vitamin C & E for 3 months is associated with a decrease of ROS as measured by flowcytometry & a variable degree of improvement in above mentioned semen parameters. KEYWORDS Reactive Oxygen Species, Male Infertility

183 ADDITION OF DIPHENYLENEIODONIUM OR DEHYDROEPIANDROSTERONE TO CULTURE MEDIA INHIBITS REACTIVE OXYGEN SPECIES PRODUCTION DURING THE EARLY CLEAVAGE STAGES OF IN VITRO-PRODUCED PORCINE EMBRYOS

2007 ◽  
Vol 19 (1) ◽  
pp. 208
Author(s):  
N. W. K. Karja ◽  
K. Kikuchi ◽  
M. Ozawa ◽  
M. Fahrudin ◽  
T. Somfai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Culture Media ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Blastocyst Stage ◽  
Control Group ◽  
Ros Production ◽  
Oxygen Species

Nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase), an enzyme required to catalyze the oxidation of NADPH to NADP during the metabolism of glucose via the pentose phosphate pathway (PPP), was considered as contributing to intracellular reactive oxygen species (ROS) production. Production of superoxide anion and H2O2 via NADPH oxidase has been reported on a rabbit blastocyst surface (Manes and Lai 1995 J. Reprod. Fertil. 104, 69–75). The objective of this study was to examine the effects on in vitro development and intracellular ROS content after the addition of diphenyleneiodonium (DPI), an inhibitor of NADPH oxidase, or dehydroepiandrosterone (DHEA), an inhibitor of glucose-6-phosphate dehydrogenase (G6PDH), to culture medium during the early embryonic development of in vitro-produced (IVP) porcine embryos. To confirm that these inhibitors lead to reduction in NADPH concentration in the embryo and hence likely to be inhibiting the PPP, a brilliant cresyl blue (BCB) test was performed on Day 2 (the day of insemination = Day 0) of culture. Porcine cumulus–oocyte complexes were matured and fertilized in vitro as described previously (Kikuchi et al. 2002 Biol. Reprod. 66, 1033–1041). Prezumptive zygotes were then cultured in NCSU-37 supplemented with 5.5 mM glucose and DPI at concentrations of 0.5 or 1 nM or DHEA at concentrations of 10 or 100 �M (DPI-0.5, DPI-1, DHEA-10 and DHEA-100 groups, respectively) from Day 0 to Day 2 of culture. All of the embryos were cultured subsequently until Day 6 in NCSU-37 supplemented with only 5.5 mM glucose. Data were analyzed by ANOVA. On Day 6, the development to the blastocyst stage of embryos in DPI-0.5, DPI-1, DHEA-10, and DHEA-100 groups were 16.1, 17.6, 16.1, and 19.5%, respectively, which were not significantly different from that of the control group (17.5%) (n d 165 per group, 5 replicates). However, the mean cell number in blastocysts derived from DPI-1, DHEA-10, and DHEA-100 groups (40.8 � 2.3, 39.3 � 1.7, and 42.5 � 2.7, respectively) was significantly higher (P &lt; 0.01) than those in the control (33.4 � 1.6) and DPI-0.5 (32.7 � 1.6) groups. At 20 min after an exposure to BCB, the percentage of BCB+ embryos in DPI-1, DHEA-10, and DHEA-100 groups (73.8, 79.9, and 77.8%, respectively) were significantly higher (P &lt; 0.01) than those in the control and DPI-0.5 groups (42% and 53.9%, respectively) (n = 81-92 per group, 6 replicates), indicating that these two inhibitors effectively induce the reduction of NADPH concentration in the embryos. Moreover, the addition of DPI at 1 nM or DHEA at 10 or 100 �M significantly decreased the H2O2 content of Day 2 embryos as compared with control embryos (n = 48-53 per group, 7 replicates). These results suggest that the addition of either DPI or DHEA to the medium during the first 2 days of culture did not impair the development of the embryos to the blastocyst stage. Decrease of cellular ROS production in Day 2 embryos in this study is interpreted as a result of inhibition of the NADPH oxidase by DPI or of the G6PDH by DHEA.

Reduced levels of intracellular reactive oxygen species and apoptotic status are not correlated with increases in cryotolerance of bovine embryos produced in vitro in the presence of antioxidants

2014 ◽  
Vol 26 (6) ◽  
pp. 797 ◽  
Author(s):  
Nathália A. S. Rocha-Frigoni ◽  
Beatriz C. S. Leão ◽  
Ériklis Nogueira ◽  
Mônica F. Accorsi ◽  
Gisele Z. Mingoti
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Control Group ◽  
Bovine Embryo ◽  
Oxygen Species ◽  
Antioxidant Supplementation ◽  
In Vitro Production ◽  
Intracellular Ros

The effects of intracellular (cysteine and β-mercaptoethanol) and extracellular (catalase) antioxidant supplementation at different times during in vitro production (IVM and/or in vitro culture (IVC)) on bovine embryo development, intracellular reactive oxygen species (ROS) levels, apoptosis and re-expansion rates after a vitrification–thawing process were examined. Blastocyst frequencies were not affected by either antioxidant supplementation (40.5%–56.4%) or the timing of supplementation (41.7%–55.4%) compared with control (48.7%; P > 0.05). Similarly, antioxidants and the moment of supplementation did not affect (P > 0.05) the total number of blastomeres (86.2–90.5 and 84.4–90.5, respectively) compared with control (85.7). However, the percentage of apoptotic cells was reduced (P < 0.05) in groups supplemented during IVM (1.7%), IVC (2.0%) or both (1.8%) compared with control (4.3%). Intracellular ROS levels measured in Day 7 blastocysts were reduced (P < 0.05) in all groups (0.60–0.78), with the exception of the group supplemented with β-mercaptoethanol during IVC (0.88), which did not differ (P > 0.05) from that in the control group (1.00). Re-expansion rates were not affected (P > 0.05) by the treatments (50.0%–93.0%). In conclusion, antioxidant supplementation during IVM and/or IVC reduces intracellular ROS and the rate of apoptosis; however, supplementation does not increase embryonic development and survival after vitrification.

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