Effect of resveratrol analogue, DMU-212, on antioxidant status and apoptosis-related genes in rat model of hepatocarcinogenesis

2016 ◽  
Vol 36 (2) ◽  
pp. 160-175 ◽  
Author(s):  
H Piotrowska ◽  
M Kujawska ◽  
M Nowicki ◽  
E Petzke ◽  
E Ignatowicz ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Mrna Expression ◽  
Messenger Rna ◽  
Mrna Level ◽  
Combined Treatment ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Protein Carbonyls ◽  
Genes Encoding ◽  
Male Wistar Rats

The aim of the study was to examine whether antioxidant properties of 3,4,4′,5-tetramethoxystilbene (DMU-212) contribute to its anticarcinogenic activity and whether DMU-212 affects the expression of apoptosis-related genes. Two-stage model of hepatocarcinogenesis was used; male Wistar rats were challenged with N-nitrosodiethylamine (NDEA), 200 mg/kg body weight (b.w.), intraperitoneal, then phenobarbital (PB) in drinking water (0.05%) was administered. Simultaneously, DMU-212 was given per os at a dose 20 or 50 mg/kg b.w. two times a week for 16 weeks. DMU-212 caused a moderate decrease in hepatic thiobarbituric acid reactive substances and protein carbonyls concentration elevated in rats treated with NDEA/PB. The activity of antioxidant enzymes examined reduced by NDEA/PB treatment was not restored in rats coadministered with DMU-212. Effects of DMU-212 on messenger RNA (mRNA) expression of antioxidant enzymes in rats challenged with NDEA/PB were diversified; no changes in their protein expression were noted in any of the groups. The expression of 17,000 genes was analyzed by Affymetrix® Rat Gene 1.1 ST Array; 15 apoptosis-related genes were selected and validated by RT-q PCR. The combined treatment with NDEA/PB and DMU-212 increased the mRNA level of some genes driving mitochondria-mediated apoptosis, whereas the mRNA expression of some anti-apoptotic genes triggering receptor-mediated apoptosis was reduced. The expression of genes encoding caspases-4, -8, -9, and -12 was also increased in rats treated with DMU-212. Although antioxidant effect of DMU-212 in rats challenged with NDEA/PB was moderate, its potential anticarcinogenic properties were demonstrated as evidenced by modulation of apoptosis-related genes.

Tissue Factor Expression in Vital Organs during Murine Traumatic Shock 

1999 ◽  
Vol 91 (6) ◽  
pp. 1844-1844 ◽  
Author(s):  
Valerie E. Armstead ◽  
Irina L. Opentanova ◽  
Alexander G. Minchenko ◽  
Allan M. Lefer
Keyword(s):  
Small Intestine ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Messenger Rna ◽  
Mrna Level ◽  
Regulatory Elements ◽  
Traumatic Shock ◽  
Surface Glycoprotein ◽  
Cell Surface Glycoprotein ◽  
Nf Kappab

Background Tissue factor (TF) is a cell-surface glycoprotein responsible for initiating the extrinsic pathway of coagulation that has been shown to have a role in the pathophysiology of sepsis and reperfusion injury. The purpose of this study was to investigate TF expression in vital organs and to determine possible regulatory mechanisms of TF expression in the lung during traumatic shock in rats. Methods Noble-Collip drum trauma was induced in anesthetized Sprague-Dawley rats. Anesthetized rats without trauma served as controls. TF activity was measured in plasma and lung tissue. TF messenger RNA (mRNA) was measured in the lung, liver, and small intestine using ribonuclease protection assays. Electromobility shift assays were used to quantify binding of nuclear extracts from lung to TF-specific consensus domains for transcription factors NF-kappaB and AP-1. Results TF activity in plasma increased up to 14-fold and +232% in the lung (P < 0.001 for plasma and lung) 2 h after trauma. TF mRNA level was significantly increased in the lungs (P < 0.01), small intestine (P < 0.01), and liver (P < 0.05) 1 h after trauma compared to sham-operated control rats. TF mRNA expression continued to increase in the lungs and the liver (both, P < 0.001) 2 h after trauma TF sequence-specific complex binding to AP-1 and NF-kappaB domains was enhanced in the lungs of trauma rats (+395%, P < 0.001 and +168%, P < 0.001, respectively). Conclusions These results suggest that TF may play an important role in the pathophysiology of severe trauma and that regulatory elements AP-1 and NF-kappaB may be involved in the regulation of TF mRNA expression in traumatic shock.

scholarly journals Thymoquinone Attenuates Diethylnitrosamine Induction of Hepatic Carcinogenesis Through Antioxidant Signaling

2010 ◽  
Vol 3 (4) ◽  
pp. 254-261 ◽  
Author(s):  
Mohamed M. Sayed-Ahmed ◽  
Abdulaziz M. Aleisa ◽  
Salim S. Al-Rejaie ◽  
Abdulaziz A. Al-Yahya ◽  
Othman A. Al-Shabanah ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Mrna Expression ◽  
Nigella Sativa ◽  
Antioxidant Properties ◽  
Cancer Chemoprevention ◽  
Thiobarbituric Acid ◽  
Albino Rats ◽  
Hepatic Carcinogenesis ◽  
Group 2 ◽  
Wistar Albino Rats

Hepatocellular carcinoma accounts for about 80–90% of all liver cancer and is the fourth most common cause of cancer mortality. Although there are many strategies for the treatment of liver cancer, chemoprevention seems to be the best strategy for lowering the incidence of this disease. Therefore, this study has been initiated to investigate whether thymoquinone (TQ),Nigella sativaderived-compound with strong antioxidant properties, supplementation could prevent initiation of hepatocarcinogenesis-induced by diethylnitrosamine (DENA), a potent initiator and hepatocarcinogen, in rats. Male Wistar albino rats were divided into four groups. Rats of Group 1 received a single intraperitoneal (I.P.) injection of normal saline. Animals in Group 2 were given TQ (4 mg/kg/day) in drinking water for 7 consecutive days. Rats of Group 3 were injected with a single dose of DENA (200 mg/kg, I.P.). Animals in Group 4 were received TQ and DENA. DENA significantly increased alanine transaminase (ALT), alkaline phosphatase (ALP), total bilirubin, thiobarbituric acid reactive substances (TBARS) and total nitrate/nitrite (NOx) and decreased reduced glutathione (GSH), glutathione peroxidase (GSHPx), glutathione-s-transferase (GST) and catalase (CAT) activity in liver tissues. Moreover, DENA decreased gene expression of GSHPx, GST and CAT and caused severe histopathological lesions in liver tissue. Interestingly, TQ supplementation completely reversed the biochemical and histopathological changes induced by DENA to the control values. In conclusion, data from this study suggest that: (1) decreased mRNA expression of GSHPx, CAT and GST during DENA-induced initiation of hepatic carcinogenesis, (2) TQ supplementation prevents the development of DENA-induced initiation of liver cancer by decreasing oxidative stress and preserving both the activity and mRNA expression of antioxidant enzymes.

scholarly journals Obesity May Provide Pro-ILC3 Development Inflammatory Environment in Asthmatic Children

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Yumin Wu ◽  
Jiawei Yue ◽  
Juncheng Wu ◽  
Wei Zhou ◽  
Dapeng Li ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Messenger Rna ◽  
Mrna Level ◽  
Asthma Severity ◽  
Lymphoid Cells ◽  
Mrna Levels ◽  
Asthmatic Children ◽  
Prevalence Of Obesity ◽  
Elevated Frequency ◽  
Relative Mrna Expression

The prevalence of obesity in children has dramatically increased in the last few decades, and obesity has also emerged as an important risk factor for asthma. Innate mechanisms have been shown to be involved in both diseases, particularly through the recently described innate lymphoid cells (ILCs), in which ILC3s have been linked to obesity both in human and in murine models. The aim of this study was to explore whether being overweight in asthmatic children was associated with elevated circulating ILC3 or elevated messenger RNA (mRNA) levels of RORC, IL-17A, and IL-22. Our results showed significantly elevated ILC3 frequencies in overweight asthmatic children compared with nonoverweight controls based on the detection of Lin+CD127+IL-23R+ cells by flow cytometry. Moreover, elevated ILC3 frequencies positively correlated with the mRNA expression of RORC which has been identified as a transcription factor of ILC3s. The relative mRNA expression level of IL-17A was also upregulated in overweight compared to nonoverweight children, as was the relative mRNA level of IL-22. However, there were no correlations between ILC3 frequencies or the expressions of RORC, IL-17A, and IL-22 and asthma severity. These results suggested that childhood obesity is an independent factor that is associated with an elevated frequency of circulating ILC3s and higher expressions of RORC, IL-22, and IL-17A.

scholarly journals Effect of Different Stages of Chronic Kidney Disease and Renal Replacement Therapies on Oxidant-Antioxidant Balance in Uremic Patients

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Hadja Fatima Tbahriti ◽  
Abbou Kaddous ◽  
Malika Bouchenak ◽  
Khedidja Mekki
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Antioxidant Enzymes ◽  
Vitamin E ◽  
Kidney Disease ◽  
Thiobarbituric Acid ◽  
Study Groups ◽  
Cardiovascular Complications ◽  
Protein Carbonyls ◽  
Severe Stage

Oxidative stress seems to be involved in the path physiology of cardiovascular complications of chronic kidney disease (CKD). In this study, we determined the effect of different stages of CKD and substitutive therapies on oxidative stress. One hundred sixty-seven patients (age:44±06years; male/female: 76/91) with CKD were divided into 6 groups according to the National Kidney Foundation classification. Prooxidant status was assessed by assaying thiobarbituric acid reactive substances, hydroperoxides, and protein carbonyls. Antioxidant defence was performed by analysis of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, vitamin E, Iron, and bilirubin. TBARS and LPO were higher in HD patients compared to other groups (P<0.001), while protein carbonyls were more increased in PD patients. The antioxidant enzymes were declined already at severe stage of CKD and they were declined notably in HD patients (P<0.001). Similar observation was found for vitamin E, Fe, and bilirubin where we observed a significant decrease in the majority of study groups, especially in HD patients (P<0.001). The evolution of CKD was associated with elevated OS. HD accentuates lipid, while PD aggravates protein oxidation. However, the activity of antioxidant enzymes was altered by impaired renal function and by both dialysis treatments.

Protective effect of chokeberry on chemical-induced oxidative stress in rat

2010 ◽  
Vol 30 (3) ◽  
pp. 199-208 ◽  
Author(s):  
Małgorzata Kujawska ◽  
Ewa Ignatowicz ◽  
Małgorzata Ewertowska ◽  
Jan Oszmiański ◽  
Jadwiga Jodynis-Liebert
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Protein Carbonyls ◽  
Thiobarbituric Acid Reactive Substances ◽  
Blood Leukocytes ◽  
Microsomal Lipid Peroxidation ◽  
Male Wistar Rats ◽  
Chokeberry Juice

Male Wistar rats were treated with chokeberry juice per os, 10 mL/kg/day, for 28 days and a single intraperitoneal (i.p.) dose of N-nitrosodiethylamine (NDEA), 150 mg/kg, or carbon tetrachloride (CCl4), 2 ml/kg. The level of hepatic microsomal lipid peroxidation, expressed as thiobarbituric acid reactive substances (TBARS), was increased in animals dosed with NDEA and CCl4. Juice pretreatment resulted in a significant decrease in TBARS by 53% and 92%, respectively. In rats administered juice alone, 50% decrease in TBARS was noted. The activities of all antioxidant enzymes were decreased in the liver of rats administered either toxicant by 29%—52% as compared to controls. Juice pretreatment resulted in an increase in the activity of catalase, glutathione peroxidase and glutathione reductase by 117%, 56% and 44%, respectively, only in rats challenged with NDEA. Although no response of plasma protein carbonyls to both toxicants was observed, the pretreatment with juice caused a 55% decrease of this parameter in CCl4—dosed rats. DNA damage in blood leukocytes induced by either toxicant was slightly reduced, by 24%, in the rats pretreated with juice and administered NDEA. The results of the study showed that pretreatment with chokeberry juice confers some protection against chemical-induced oxidative stress.

scholarly journals Protective Effect of Dorema glabrum on Induced Oxidative Stress by Diazinon in Hippocampus of Rat

2019 ◽  
pp. 1-7
Author(s):  
Mina Adampourezare ◽  
Parisa Sistani ◽  
Homeira Hatami Nemati
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Catalase Activity ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Male Wistar Rats ◽  
Pre Treatment

Introduction: Diazinon (DZN) administration produces lipid peroxidation as an indicator of oxidative stress in the brain. Some medicinal plants such as Dorema glabrum has antioxidant properties, so can be used as an antioxidant that may protect neurons from oxidative stress. The aim of present study was to investigate the effect of D. glabrum against DZN-induced oxidative stress in hippocampus. Methods: Twenty-four adult male Wistar rats were used in this study. The rats randomly were divided into four groups including a control group, and two groups received different doses of D. glabrum (40 and 80 mg/kg) as pre-treatment for 21 days with DZN (100 mg/Kg) that was injected intraperitoneally (ip) in last day of D. glabrum usage, and one group received only DZN. Thiobarbituric acid reactive substances (TBARS), which are the indicators of lipid peroxidation, and the activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase and catalase) were determined in the ratsʼ hippocampus. Results: Administration of DZN significantly increased TBARS levels and superoxide dismutase activity and decreased glutathione peroxidase activity but there were no significant changes in catalase activity in the hippocampus. Combined D. glabrum and DZN treatment, caused a significant increase in glutathione peroxidase, a significant decrease of TBARS and a significant decrease in superoxide dismutase and again no significant changes in catalase activity in the rats’ hippocampus when compared to the rats treated with DZN. Conclusion: Our study demonstrated that D. glabrum had an amelioratory effect on oxidative stress induced by DZN.

scholarly journals Hypoglycemic and Antioxidant Effects of Subcoriacin in Normal and Streptozotocin-induced Diabetic Rats

2019 ◽  
Vol 54 (4) ◽  
Author(s):  
José M. Narváez-Mastache ◽  
Claudia Soto ◽  
Guillermo Delgado
Keyword(s):  
Antioxidant Enzymes ◽  
Blood Glucose ◽  
Antioxidant Activities ◽  
Combined Treatment ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Endogenous Antioxidant

Subcoriacin (1) is a 3-aryl-6-prenylcoumarin isolated from Eysenhardtia subcoriacea that has shown antioxidant activity in vitro, and has shown to scavenge free radicals and also to improve the reduced glutathione levels in pancreatic homogenates. The present investigation evaluates the protective effect of 1 against oxidative injury in normal and streptozotocin (STZ)-induced diabetic rats. The i.p. administration of 1 at a dose of 100 mg/kg body weight for 5 d, significantly decreased blood glucose levels and improved the endogenous antioxidant system. Also, a significant increase in the activities of the antioxidant enzymes glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) occurred. Combined treatment of rats with 1 (100 mg/kg) and STZ significantly reduced the pancreatic levels of thiobarbituric acid reactive substances (TBARS) levels. Likewise, significant increases in the activities of the antioxidant enzymes together with a decrease in blood glucose levels in both treatments were observed. The results demonstrate and support the relationship between the hypoglycemic and antioxidant activities displayed by the natural compound 1.

Liraglutide Ameliorates Lipotoxicity-Induced Oxidative Stress by Activating the NRF2 Pathway in HepG2 Cells

2020 ◽  
Vol 52 (07) ◽  
pp. 532-539 ◽  
Author(s):  
Chong-gui Zhu ◽  
Ying Luo ◽  
Hao Wang ◽  
Jun-Yi Li ◽  
Jie Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Mrna Expression ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Nuclear Translocation ◽  
Thiobarbituric Acid ◽  
Related Factor ◽  
Protective Effects ◽  
Alcoholic Fatty Liver

AbstractAlthough glucagon-like peptide-1 (GLP-1) analogue has been reported to suppress oxidative stress in non-alcoholic fatty liver disease (NAFLD), an effective therapeutic agent for NAFLD is currently unavailable. Therefore, in this study, we aimed to investigate the protective effects of the GLP-1 analogue liraglutide against lipotoxicity-induced oxidative stress in HepG2 cells and to elucidate the underlying mechanisms. HepG2 cells were cultured for 48 hours and treated with a free fatty acid (FFA) mixture: FFA mixture and liraglutide or FFA mixture, liraglutide, and exendin (9–39). Lipid accumulation was examined by oil red O staining. Oxidative stress was assessed by measuring the levels of intracellular reactive oxygen species using 2′,7′-dichlorofluorescein diacetate and thiobarbituric acid-reactive substances, whereas antioxidant capacity was assessed by measuring the activity of superoxide dismutase and catalase. Expression of the nuclear factor erythroid-2-related factor 2 (NRF2) gene and the genes encoding antioxidant enzymes was analyzed using quantitative RT-PCR. Cellular and nuclear NRF2 expression levels were assessed using immunofluorescence cell staining and western blotting. Liraglutide treatment reduced high fat-induced lipid formation and the levels of oxidative stress markers and increased antioxidant enzyme activity in HepG2 cells. Liraglutide treatment increased the mRNA expression of NRF2 target genes, induced NRF2 nuclear translocation, and increased nuclear NRF2 levels without altering NRF2 mRNA expression. Collectively, these results indicate that liraglutide exhibits a protective effect against lipotoxicity-induced oxidative stress, possibly via modulation of NRF2 and expression of antioxidant enzymes in liver cells.

scholarly journals Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Hiroshi Nagahisa ◽  
Kazumi Ikezaki ◽  
Ryotaro Yamada ◽  
Takashi Yamada ◽  
Hirofumi Miyata
Keyword(s):  
Mrna Expression ◽  
Muscle Damage ◽  
Satellite Cell ◽  
Muscle Pain ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Mrna Level ◽  
Eccentric Contraction ◽  
Vigorous Exercise ◽  
Male Wistar Rats

Inexperienced vigorous exercise, including eccentric contraction (ECC), causes muscle pain and damage. Similar prior light exercise suppresses the development of muscle pain (repeated-bout effect), but the molecular mechanisms behind this are not sufficiently understood. In this study, the influence of a nondamaging preconditioning ECC load (Precon) on muscle pain-related molecules and satellite cell-activating factors was investigated at the mRNA expression level. Nine-week-old male Wistar rats (n=36) were divided into 2 groups: a group receiving only a damaging ECC (100 contractions) load (non-Precon) and a group receiving a nondamaging ECC (10 contractions) load 2 days before receiving the damaging ECC load (Precon). ECC was loaded on the left leg, and the right leg was regarded as the intact control (CTL). The medial head of the gastrocnemius muscle from all rats was excised 2 or 4 days after the damaging ECC loading, and the relative mRNA expression levels of muscle pain- and satellite cell-related molecules were quantitated using real-time RT PCR. Precon suppressed increases in MHC-embryonic and MHC-neonatal mRNA expressions. Enhancement of HGF, Pax7, MyoD, and myogenin mRNA expression was also suppressed, suggesting that Precon decreased the degree of muscle damage and no muscle regeneration or satellite cell activation occurred. Similarly, increases in mRNA expression of muscle pain-related molecules (BKB2 receptor, COX-2, and mPGEC-1) were also suppressed. This study clearly demonstrated that at the mRNA level, prior light ECC suppressed muscle damage induced by later damaging ECC and promoted recovery from muscle pain.

Effects of Antioxidant Supplementation and Exercise Training on Erythrocyte Antioxidant Enzymes

2006 ◽  
Vol 76 (5) ◽  
pp. 324-331 ◽  
Author(s):  
Marsh ◽  
Laursen ◽  
Coombes
Keyword(s):  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Endurance Training ◽  
Young Male ◽  
Antioxidant Defenses ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Supplementation ◽  
Male Wistar Rats ◽  
Exercise Induced ◽  
Antioxidant Supplements

Erythrocytes transport oxygen to tissues and exercise-induced oxidative stress increases erythrocyte damage and turnover. Increased use of antioxidant supplements may alter protective erythrocyte antioxidant mechanisms during training. Aim of study: To examine the effects of antioxidant supplementation (α-lipoic acid and α-tocopherol) and/or endurance training on the antioxidant defenses of erythrocytes. Methods: Young male Wistar rats were assigned to (1) sedentary; (2) sedentary and antioxidant-supplemented; (3) endurance-trained; or (4) endurance-trained and antioxidant-supplemented groups for 14 weeks. Erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities, and plasma malondialdehyde (MDA) were then measured. Results: Antioxidant supplementation had no significant effect (p > 0.05) on activities of antioxidant enzymes in sedentary animals. Similarly, endurance training alone also had no effect (p > 0.05). GPX (125.9 ± 2.8 vs. 121.5 ± 3.0 U.gHb–1, p < 0.05) and CAT (6.1 ± 0.2 vs. 5.6 ± 0.2 U.mgHb–1, p < 0.05) activities were increased in supplemented trained animals compared to non-supplemented sedentary animals whereas SOD (61.8 ± 4.3 vs. 52.0 ± 5.2 U.mgHb–1, p < 0.05) activity was decreased. Plasma MDA was not different among groups (p > 0.05). Conclusions: In a rat model, the combination of exercise training and antioxidant supplementation increased antioxidant enzyme activities (GPX, CAT) compared with each individual intervention.

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