Abstract 253: Di-n-butyl Phthalate: An Indoor Pollutant Induces Murine Macrophages Oxidative Stress and Inflammation, a Potential Atheropathogenesis Modulator

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Zahra Mazhar ◽  
Dhuha Alsayrafi ◽  
Tong Wu ◽  
Mahdi Garelnabi
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Tnf Alpha ◽  
Gene Expressions ◽  
Compensatory Response ◽  
Murine Macrophages ◽  
Atherosclerosis Progression ◽  
Indoor Pollutant ◽  
Human Cardiovascular System ◽  
Butyl Phthalate

Di-n-butyl phthalate (DBP) is used in air fresheners. It is a colorless oily compound which also used for manufacturing bendable plastics. DBP can cause low acute or chronic toxicity; however, the effect of DBP on humans in the form of air fresheners is not well studied. The effect of DBP on the human cardiovascular system has not been studied. Macrophages are involved in atherosclerosis progression and development; murine macrophages (RAW 264.7) were used for this study. The macrophages were treated with 10uM, 20uM and 50uM DBP for 6 hours, 12 hours and 24 hours. Genes involved in inflammation and antioxidant activity like TNF-a, MCP-1, VCAM-1, NF-kB, PON1, SOCS were analyzed after treatment. macrophages showed statistically significant increases in TNF-alpha expression (p≤ 0.05) after 24 hour treatment with DBP. The expression of NF-kB showed a significant increase in response to DBP treatment (p≤ 0.05) at 24 hours. MCP-1 and VCAM-1 gene expressions were also upregulated after exposure to DBP. Interestingly, catalase gene expression was upregulated in all treatments after 24 hours of exposure however PON-1 gene expression showed differential upregulation responses. Our data clearly suggest that DBP induces inflammation in macrophages. PON1 and catalase upregulated gene expression indicative of a compensatory response to oxidative stress associated with the treatment. Oxidative stress and inflammation mediated macrophages responses strongly linked to atherosclerosis pathogenesis.

Chemoprotective Effects of Propolis on Aflatoxin B1-Induced Hepatotoxicity in Rats: Oxidative Damage and Hepatotoxicity by Modulating TP53, Oxidative Stress

2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Oxidative Damage ◽  
Aflatoxin B1 ◽  
Tp53 Gene ◽  
Control Group ◽  
Glutathione S Transferase ◽  
Gene Expressions ◽  
Cat Gene ◽  
Gst Activity

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.

scholarly journals Effects of glutamine supplementation on oxidative stress-related gene expression and antioxidant properties in rats with streptozotocin-induced type 2 diabetes

2011 ◽  
Vol 107 (8) ◽  
pp. 1112-1118 ◽  
Author(s):  
Pei-Hsuan Tsai ◽  
Jun-Jen Liu ◽  
Chui-Li Yeh ◽  
Wan-Chun Chiu ◽  
Sung-Ling Yeh
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Amino Acid ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Enzyme Activities ◽  
Antioxidant Enzyme Activities ◽  
Related Gene ◽  
Gene Expressions ◽  
Oxidative Stress Related Gene

There are close links among hyperglycaemia, oxidative stress and diabetic complications. Glutamine (GLN) is an amino acid with immunomodulatory properties. The present study investigated the effect of dietary GLN on oxidative stress-relative gene expressions and tissue oxidative damage in diabetes. There were one normal control (NC) and two diabetic groups in the present study. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin (STZ). Rats in the NC group were fed a regular chow diet. In the two diabetic groups, one group (diabetes mellitus, DM) was fed a common semi-purified diet while the other group received a diet in which part of the casein was replaced by GLN (DM-GLN). GLN provided 25 % of total amino acid N. The experimental groups were fed the respective diets for 8 weeks, and then the rats were killed for further analysis. The results showed that blood thioredoxin-interacting protein (Txnip) mRNA expression in the diabetic groups was higher than that in the NC group. Compared with the DM group, the DM-GLN group had lower glutamine fructose-6-phosphate transaminase 1, a receptor of advanced glycation end products, and Txnip gene expressions in blood mononuclear cells. The total antioxidant capacity was lower and antioxidant enzyme activities were altered by the diabetic condition. GLN supplementation increased antioxidant capacity and normalised antioxidant enzyme activities. Also, the renal nitrotyrosine level and Txnip mRNA expression were lower when GLN was administered. These results suggest that dietary GLN supplementation decreases oxidative stress-related gene expression, increases the antioxidant potential and may consequently attenuate renal oxidative damage in rats with STZ-induced diabetes.

scholarly journals The Influence of Photoperiod on the Action of Exogenous Leptin on Gene Expression of Proinflammatory Cytokines and Their Receptors in the Thoracic Perivascular Adipose Tissue (PVAT) in Ewes

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Agata Krawczyńska ◽  
Andrzej P. Herman ◽  
Hanna Antushevich ◽  
Joanna Bochenek ◽  
Karolina Wojtulewicz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Proinflammatory Cytokines ◽  
Leptin Resistance ◽  
Control Treatment ◽  
Natural Phenomenon ◽  
Gene Expressions ◽  
Perivascular Adipose Tissue ◽  
Endothelium Dysfunction ◽  
Atherosclerosis Progression

Leptin resistance is either a condition induced by human obesity or a natural phenomenon associated with seasonality in ruminants. In the cardiovascular system, the leptin resistance state presence is a complex issue. Moreover, the perivascular adipose tissue (PVAT) appears to be crucial as a source of proinflammatory cytokines and as a site of interaction for leptin contributing to endothelium dysfunction and atherosclerosis progression. So the aim of this study was to examine the influence of the photoperiod on the action of exogenous leptin on gene expression of selected proinflammatory cytokines and their receptors in thoracic PVAT of ewe with or without prior lipopolysaccharide (LPS) stimulation. The experiment was conducted on 48 adult, female ewes divided into 4 group (n=6 in each): control, with LPS intravenous (iv.) injection (400 ng/kg of BW), with leptin iv. injection (20 μg/kg BW), and with LPS and 30-minute-later leptin injection, during short-day (SD) and long-day (LD) seasons. Three hours after LPS/control treatment, animals were euthanized to collect the PVAT adherent to the aorta wall. The leptin injection enhanced IL1B gene expression only in the LD season; however, in both seasons leptin injection intensified LPS-induced increase in IL1B gene expression. IL1R2 gene expression was increased by leptin injection only in the SD season. Neither IL6 nor its receptor and signal transducer gene expressions were influenced by leptin administration. Leptin injection increased TNFA gene expression regardless of photoperiodic conditions. Only in the SD season did leptin treatment increase the gene expression of both TNFα receptors. To conclude, leptin may modulate the inflammatory reaction progress in PVAT. In ewe, the sensitivity of PVAT on leptin action is dependent upon the photoperiodic condition with stronger effects stated in the SD season.

scholarly journals The effect of Kappaphycus alvarezii active fraction on oxidative stress and inflammation in streptozotocin and nicotinamide-induced diabetic rats

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Evy Yulianti ◽  
Sunarti ◽  
Mae Sri Hartati Wahyuningsih
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Kappaphycus Alvarezii ◽  
Male Rats ◽  
Diabetic Rat ◽  
Potential Candidate ◽  
Active Fraction ◽  
Gene Expressions ◽  
Nadph Oxidase 4

Abstract Background High glucose concentration increases the glycation process which leads to oxidative stress and inflammation, that can cause complications in diabetes. Several medicinal plants have been used in the treatment of diabetes and its complications. One of them is Kappaphycus alvarezii, an algae that has known antidiabetic abilities. This study aimed to examine the effect of K. alvarezii active fraction on plasma hydrogen peroxide (H2O2) and Tumor Necrosis Factor α (TNFα) levels, renal NADPH oxidase 4 (NOX4) and Nuclear Factor κ B (NFκB) gene expressions. Methods Active fraction was obtained from bioassay-guided fractionation with antiglycation ability. In vivo study was performed on twenty Wistar male rats. The level of H2O2 was measured using H2O2 Assay Kit, the Optical Density value measured using spectrophotometer at a wavelength of 405 nm. Plasma TNFα level was measured using ELISA. Renal NOX4 and NFκB gene expression was analyzed using qPCR. Results Active fraction significantly reduced plasma H2O2 but not TNFα levels. Furthermore, renal NOX4 gene expression was lower in the diabetic rat group treated with active fraction compared to the untreated group but not NFκB gene expression. Conclusions K. alvarezii active fraction has an activity to reduce plasma H2O2 as well as renal NOX4 gene expression. Therefore, this fraction could be developed as a potential candidate for diabetes treatment through oxidative stress mechanisms.

scholarly journals Differential Oxidative Stress Responses to D-Galactosamine-Lipopolysaccharide Hepatotoxicity Based on Real Time PCR Analysis of Selected Oxidant/Antioxidant and Apoptotic Gene Expressions in Rat

2011 ◽  
pp. 549-558 ◽  
Author(s):  
N. LEKIĆ ◽  
D. ČERNÝ ◽  
A. HOŘÍNEK ◽  
Z. PROVAZNÍK ◽  
J. MARTÍNEK ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Stress Responses ◽  
Caspase 3 ◽  
Histological Evaluation ◽  
Pcr Analysis ◽  
Heme Oxygenase 1 ◽  
Gene Expressions ◽  
Glutathione Peroxidase 1 ◽  
Apoptotic Pathways

Oxidative stress and apoptosis are proposed mechanisms of cellular injury in studies of xenobiotic hepatotoxicity. This study is focused on addressing the mutual relationship and early signals of these mechanisms in the D-galactosamine and lipopolysaccharide (D-GalN/LPS) hepatotoxicity model, with the help of standard liver function and biochemistry tests, histology, and measurement of gene expression by RT-PCR. Intraperitoneal injection of 400 mg/kg D-GalN and 50 μg/kg LPS was able to induce hepatotoxicity in rats, as evidenced by significant increases in liver enzymes (ALT, AST) and raised bilirubin levels in plasma. Heme oxygenase-1 and nitric oxide synthase-2 gene expressions were significantly increased, along with levels of their products, bilirubin and nitrite. The gene expression of glutathione peroxidase 1 remained unchanged, whereas a decrease in superoxide dismutase 1 gene expression was noted. Furthermore, the significant increase in the gene expression of apoptotic genes Bid, Bax and caspase-3 indicate early activation of apoptotic pathways, which was confirmed by histological evaluation. In contrast, the measured caspase-3 activity remained unchanged. Overall, the results have revealed differential oxidative stress and apoptotic responses, which deserves further investigations in this hepatotoxicity model.

Fish oil feeding alters liver gene expressions to defend against PPARα activation and ROS production

2002 ◽  
Vol 282 (2) ◽  
pp. G338-G348 ◽  
Author(s):  
Mayumi Takahashi ◽  
Nobuyo Tsuboyama-Kasaoka ◽  
Teruyo Nakatani ◽  
Masami Ishii ◽  
Shuichi Tsutsumi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Fatty Acid ◽  
Fish Oil ◽  
Uncoupling Protein ◽  
Favorable Effect ◽  
Safflower Oil ◽  
Gene Expressions ◽  
Antioxidant Genes ◽  
Fish Oil Diet

Fish oil rich in n-3 polyunsaturated fatty acids has been shown to reduce the risk of cardiovascular diseases partly by reduction of blood triglyceride concentration. This favorable effect mainly results from the combined effects of inhibition of lipogenesis by decrease of SREBP-1 and stimulation of fatty acid oxidation by activation of peroxisome proliferator-activated receptor-α (PPARα) in liver. However, because fish oil is easily peroxidized to form hydroperoxides and increases oxidative stress, some defense mechanism(s) against oxidative stress might occur. To understand these complex effects of fish oil diet, the gene expression profile of mice liver was analyzed using high-density oligonucleotide arrays. High-fat diet (60% of total energy intake) as either safflower oil or fish oil (tuna) was given to mice. After 6 mo of feeding, expression levels of a total of 6,521 genes were analyzed. In fish oil diet compared with safflower oil diet, immune reaction-related genes, antioxidant genes (several glutathione transferases, uncoupling protein 2, and Mn-superoxide dismutase), and lipid catabolism-related genes upregulated, whereas cholesterol and fatty acid synthesis-related genes and 17-alpha hydroxylase/C17–20 lyase and sulfotransferases related to production of endogenous PPARα ligands and reactive oxygen species (ROS) downregulated markedly. Because upregulation of these antioxidant genes and downregulation of sulfotransferases were also observed in mice administered fenofibrate, altered gene expression related to antioxidant system observed in fish oil feeding was mediated directly and indirectly by PPARα activation. However, downregulation of 17-alpha hydroxylase/C17–20 lyase was not due to PPARα activation. These data indicate that fish oil feeding downregulated the endogenous PPARα-activation system and increased antioxidant gene expressions to protect against ROS excess.

scholarly journals CMP-Neu5Ac Hydroxylase Null Mice as a Model for Studying Metabolic Disorders Caused by the Evolutionary Loss of Neu5Gc in Humans

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Deug-Nam Kwon ◽  
Yun-Jung Choi ◽  
Ssang-Goo Cho ◽  
Chankyu Park ◽  
Han Geuk Seo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Mitochondrial Dysfunction ◽  
Metabolic Disorders ◽  
Tca Cycle ◽  
Liver Weight ◽  
Pentose Phosphate ◽  
Sirtuin 1 ◽  
Null Mouse ◽  
Gene Expressions

The purpose of this study was to identify the modification/turnover of gene products that are altered in humans due to evolutionary loss of Neu5Gc. CMP-Neu5Ac hydroxylase- (Cmah-) deficient mice show the infiltration of Kupffer cells within liver sinusoids, whereas body and liver weight develop normally. Pathway analysis by use of Illumina MouseRef-8 v2 Expression BeadChip provided evidence that a number of biological pathways, including the glycolysis, gluconeogenesis, TCA cycle, and pentose phosphate pathways, as well as glycogen metabolism-related gene expression, were significantly upregulated inCmah-null mice. The intracellular glucose supply inCmah-null mice resulted in mitochondrial dysfunction, oxidative stress, and the advanced glycation end products accumulation that could further induce oxidative stress. Finally, lowsirtuin-1andsirtuin-3gene expressions due to higher NADH/NAD inCmah-null mice decreasedFoxo-1andMnSODgene expression, suggesting that oxidative stress may result in mitochondrial dysfunction inCmah-null mouse. The present study suggests that mice with CMAH deficiency can be taken as an important model for studying metabolic disorders in humans.

Antagonistic Property of G2013 (α-L-Guluronic Acid) on Gene Expression of MyD88, Tollip, and NF-κB in HEK293 TLR2 and HEK293 TLR4

2019 ◽  
Vol 19 (2) ◽  
pp. 144-149 ◽  
Author(s):  
Laleh Sharifi ◽  
Asghar Aghamohammadi ◽  
Somaye Aletaha ◽  
Razieh Bigdeli ◽  
Vahid Asgary ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cell Lines ◽  
Low Dose ◽  
Signaling Cascade ◽  
High Dose ◽  
Quantitative Real Time Pcr ◽  
Gene Expressions ◽  
Guluronic Acid ◽  
Immunosuppressive Property

Introduction: Inhibition of Toll-like receptors (TLRs) signaling plays a crucial role in suppressing the inflammation and available data presenting G2013 as an immunomodulatory agent, therefore, we designed this study to answer whether G2013 can affect the signaling pathway of TLR2 and TLR4. Methods: Cytotoxicity study of G2013 was performed by MTT assay. HEK293 TLR2 and HEK293 TLR4 cell lines were cultured and treated with low dose (5µg/ml) and high dose (25µg/ml) of G2013 for 24 hours. Gene expressions of MyD88, Tollip, and NF-κB were defined by quantitative real-time PCR. Results: The cytotoxicity assay showed that the concentrations lesser than 125μg/ml of G3012 had no apparent cytotoxicity, however, the concentrations of 5µg/ml and 25µg/ml could suppress the mRNA expression of MyD88, Tollip and NF-κB in HEK293 TLR2 and HEK293 TLR4 cell lines. Conclusion: in our study, we verified the linkage between the immunosuppressive property of G2013 and TLR2, TLR4 signaling cascade; but so far, the specific target of G2013 and its molecular mechanism has not been detected yet. We recommend further studies on other Patten Recognition Receptors (PRRs)and other mechanisms of inflammation like oxidative stress to be conducted in the future.

Abstract P426: Quercetin Intake Differentially Affects the Plasma Lipid Levels and Lipoproteins Associated Gene Expression in Normal C57bl Female Mice

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Mahdi Garelnabi ◽  
Halleh Mahini
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Beneficial Effect ◽  
Plasma Lipids ◽  
Plasma Lipid ◽  
Exercise Group ◽  
Normal Female ◽  
Lipid Levels ◽  
Gene Expressions ◽  
Female Mice

Background: Quercetin is a member of the bioflavonoids family known to have antiatherogenic, antiinflammatory, and antihypertensive properties; and reported to have cardiovascular protective role. Quercetin through its antioxidant action may protect against oxidative stress induced by free radicals consequently decreasing the potential for modification of low density lipoprotein cholesterol (LDL); however it is not clear if the intake of quercetin during exercise may have beneficial effect on plasma lipids. Goals and hypothesis: We hypothesized that the intake of quercetin with exercise will affect plasma lipids. The goal of this study is to investigate the beneficial effect of Quercetin on normal female mice. Study Design and Methods: We investigated the possible beneficial effects of the combined exercise and quercetin on plasma lipids in C57BL6 normal female mice fed normal mouse chow. Mice (N=29) were divided into four groups. These groups are as follows: Control mice, left untreated; control quercetin group, orally supplied with 100 μg/day of quercetin without exercising; exercise group without quercetin, and exercise group with quercetin supplements. The exercise groups were run on a treadmill for 30 minutes, 15m/m/ 5 days/week for 30 days. At the end of the month of the treatment, mice were sacrificed liver gene expressions for genes associated with lipoprotein metabolism were analyzed, and plasma lipids levels were analyzed. Results and Discussion: Our data interestingly showed that Quercetin differentially influences the levels of lipoprotein, oxidative stress and inflammatory markers gene expression during exercise in normal female mice; however plasma lipids, specifically TG plasma levels have elevated among mice consuming quercetin alone or with exercise significantly (P<0.5). Conclusion: This study have demonstrated that Quercetin intake with exercise may differentially affects the plasma lipid levels and lipoproteins associated gene expression in normal C57BL female mice.

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