Benefical effects of lycopene against contrast medium-induced oxidative stress, inflammation, autophagy, and apoptosis in rat kidney

2014 ◽  
Vol 34 (5) ◽  
pp. 487-496 ◽  
Author(s):  
M Buyuklu ◽  
FM Kandemir ◽  
M Ozkaraca ◽  
T Set ◽  
EM Bakirci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Kidney ◽  
Inflammatory Cells ◽  
Control Group ◽  
Albino Rats ◽  
Related Complication ◽  
Wistar Albino Rats ◽  
Oxide Synthase ◽  
Preventive Effects ◽  
Inducible Nitric Oxide

Currently, the number of imaging and interventional procedures that use contrast agents (CAs) is gradually increasing. Contrast-induced nephropathy (CIN) is the most important CA-related complication. Oxidative stress plays a significant role in its pathophysiology. Lycopene (LPN) is a natural substance with strong antioxidant capacity. The present study aimed to investigate the potential preventive effects of LPN against CIN. In total, 28 male Wistar albino rats were divided into 4 groups with 7 rats in each group; the groups include normal control group, LPN only group at a dose of 4 mg/kg/day for 10 days, CIN group by administering 10 mg/kg furosemide IM + 10 mg/kg indomethacin IP + 10 ml/kg iomeprol IV following 24-h dehydration, and CIN + LPN group. There were statistically significant increase in urea, creatinine, and malondialdehyde levels ( p < 0.001, for all) but a significant decrease in glutathione, superoxide dismutase, catalase, and glutathione peroxidase levels ( p < 0.001, for all) in the CIN group compared with the control group. On histological examination, a significant increase of infiltrated inflammatory cells and necrotic degenerative changes were observed in the CIN group and the immunohistochemical examination revealed a significant increase in inflammation (inducible nitric oxide synthase), autophagy (LC3/B), and apoptosis (cleaved caspase 3) in the CIN group compared with the control group ( p < 0.05, for all). Significant improvements in these unfavorable parameters were observed with CIN + LPN group compared with the CIN only group. In conclusion, the favorable effects of LPN as an anti-inflammatory, antiautophagic, and antiapoptotic agent in an experimental model of CIN have been demonstrated.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclosporin A ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Mechanism ◽  
Antioxidant Parameters ◽  
Group 2 ◽  
Wistar Albino Rats

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

scholarly journals Effects of Safranal on Tissue Oxidative Stress in Sub-Chronic Thinner-Addicted Rats

2020 ◽  
Vol 71 (1) ◽  
pp. 1997
Author(s):  
M. DÜZ ◽  
A. F. FIDAN
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Total Antioxidant Capacity ◽  
Reduced Glutathione ◽  
Control Group ◽  
Albino Rats ◽  
Total Antioxidant ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

The present study was carried out to determine the effects of sub-chronic thinner addiction on the oxidant-antioxidant balance and oxidative stress on certain tissues and the possible protective effect of safranal against thinner toxication in rats. Adult male Wistar albino rats were randomly divided into four groups of 10 animals each as follows: control (C), safranal (S), thinner (T) and thinner+safranal (T+S). The control group received 1cc saline by gastric gavage. Safranal was administered to S and T+S groups by using gastric gavage at a dose of 100 mg/kg/day and volume of 0.1 mL/kg/day. Thinner inhalation was applied to T and T+S groups in a container with NaOH tablets twice a day. Levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NOx) metabolites, total antioxidant capacity (TAS) and total oxidant capacity (TOS) were determined in liver, lung, brain, kidney and testis tissues of the rats. In the T+S group, it was observed that the MDA levels significantly decreased in all tissues, except the kidney, in comparison to the thinner inhalation group (p = 0.000). When the NOx levels of the T+S group were compared with the levels of the T group, it was concluded that there existed a statistically significant decrease in the NOx levels in alltissues (p = 0.000). In T+S group, it was observed that safranal either eliminated or mitigated oxidative stress that developed in tissues through decreasing MDA and TOS levels and increasing GSH and TAS levels and caused significant decreases in NOX levels in all tissues. As a result, it was determined that safranal, although not uniform for all tissue types, had a protective potential against the damaging effects of oxidative stress caused by sub-chronic thinner inhalation.

scholarly journals The Effects of Pomegranate and Carvacrol on Methotrexate-Induced Bone Marrow Toxicity in Rats

2014 ◽  
Vol 37 (2) ◽  
pp. 93 ◽  
Author(s):  
Velat Şen ◽  
Mehtap Bozkurt ◽  
Sevda Söker ◽  
Aydın Ece ◽  
Ali Güneş ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Hematological Parameters ◽  
Control Group ◽  
Albino Rats ◽  
Bone Marrow Toxicity ◽  
Group 4 ◽  
Bone Marrow Damage ◽  
Group 2 ◽  
Wistar Albino Rats

Purpose: The aim of this study was to evaluate the effects of pomegranate (PMG) extract and carvacrol (CARV) on methotrexate (MTX)-induced oxidative stress and bone marrow toxicity. Methods: Wistar albino rats (32 rats) were divided into four groups (n=8): Group 1 was control; Group 2 was given a single intraperitoneal injection of methotrexate (20 mg/kg); Group 3 was treated with carvacrol (73 mg/kg i.p.) one day before MTX (20 mg/kg i.p.) injection; and, Group 4 received a single dose of MTX (20 mg/kg i.p) while PMG was administered orally for seven days at 225 mg/kg. After animals were euthanized, blood samples were taken to evaluate hematological parameters and oxidative stress. In addition, the femur was cropped and bone marrow was extracted for examination. Results: White blood cell count, hemoglobin, hematocrit and platelet count were found to be decreased in the MTX group, but these changes were prevented in the groups that received CARV and PMG. Furthermore, decreased bone marrow cellularity was found in the groups treated with MTX, whereas the PMG and CARV groups had cellularity similar to controls. Strikingly, oxidative stress increased in the MTX group, but was ultimately decreased in the rats that received the antioxidants PMG and CARV. Conclusion: Carvacrol and PMG were found to be protective against methotrexate-induced oxidative bone marrow damage. Use of these antioxidants, in combination with chemotherapeutics, may help to reduce some adverse effects of methotrexate.

scholarly journals Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Gadah Albasher ◽  
Asma S. Alsaleh ◽  
Nourah Alkubaisi ◽  
Saleh Alfarraj ◽  
Saad Alkahtani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neuroprotective Effect ◽  
Interleukin 1 ◽  
Physiological Saline ◽  
Acetylcholinesterase Activity ◽  
Control Group ◽  
Albino Rats ◽  
Cortical Damage ◽  
Wistar Albino Rats ◽  
Oxide Synthase

Organophosphorus insecticides including chlorpyrifos (CPF) are mainly used for agriculture, household, and military purposes; their application is associated with various adverse reactions in animals and humans. This study was conducted to evaluate the potential neuroprotective effect of red beetroot methanolic extract (RBR) against CPF-induced cortical damage. Twenty-eight adult male Wistar albino rats were divided into 4 groups (n=7 in each group): the control group was administered physiological saline (0.9% NaCl), the CPF group was administered CPF (10 mg/kg), the RBR group was administered RBR (300 mg/kg), and the RBR+CPF group was treated with RBR (300 mg/kg) 1 hr before CPF (10 mg/kg) supplementation. All groups were treated for 28 days. Rats exposed to CPF exhibited a significant decrease in cortical acetylcholinesterase activity and brain-derived neurotrophic factor and a decrease in glial fibrillary acidic protein. CPF intoxication increased lipid peroxidation, inducible nitric oxide synthase expression, and nitric oxide production. This was accompanied by a decrease in glutathione content and in the activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase in the cortical tissue. Additionally, CPF enhanced inflammatory response, indicated by increased levels and expression of interleukin-1β and tumor necrosis factor-α. CPF triggered neuronal apoptosis by upregulating Bax and caspase-3 and downregulating Bcl-2. However, RBR reversed the induced neuronal alterations following CPF intoxication. Our findings suggest that RBR can minimize and prevent CPF neurotoxicity through its antioxidant, anti-inflammatory, and antiapoptotic activities.

scholarly journals ANALYSIS OF OXIDATIVE STRESS MARKERS IN CHRONIC CONSUMPTION OF MONOSODIUM GLUTAMATE ON LIVER OF WISTAR ALBINO RATS

2021 ◽  
pp. 116-119
Author(s):  
SURENDRA BABU THANGACHI ◽  
VARSHA SRIRAM MOKHASI ◽  
AGA AMMAR MURTHUZA
Keyword(s):  
Oxidative Stress ◽  
Monosodium Glutamate ◽  
Liver Homogenate ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Albino Rats ◽  
High Dose ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Wistar Albino Rats

Objective: The study was intended to explore whether Monosodium glutamate (MSG) induces oxidative stress on the liver of Wistar albino rats when fed chronically at three different doses, namely, low, mid, and high doses identical to human consumption doses in growing countries. Methods: The acclimatized Wistar albino rats (n=24) were randomly selected and grouped into four groups, namely Control, Low dose MSG (180 mg kg), Mid dose MSG (360 mg/kg), and High dose MSG (720 mg/kg). The animals were orally administered MSG for 120 days. After completion of the experimental period (120 days), euthanized animal liver was homogenized to investigate the oxidative stress marker enzymes such as Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx), Catalase (CAT), and Myeloperoxidase (MPO). Results: The MPO showed a significant increase (p<0.05) in liver homogenate of all MSG induced groups when compared to control group. The SOD, CAT, and GPx activity deteriorated (p<0.05) in monosodium induced groups contrasting to the control group. Conclusion: The effects of MSG on oxidative stress markers on liver homogenate in the current study exhibited erratic abnormal changes in oxidative stress markers of monosodium induced groups which contemplate the harmful effects of MSG consumed chronically. The further studies should confirm the genetic basis of oxidative stress damage and transform the safety regulations of MSG consumption throughout the world.

scholarly journals Nutrient, Bioactive Components and Effects of Ethanol Extracts of Annona muricata Leaves and Fagara zanthoxyloide Roots on Zidovudine-Induced Oxidative Stress in Wistar Rats

2019 ◽  
pp. 1-11
Author(s):  
O. U. Ekere ◽  
C. C. Monago-Ighorodje ◽  
C. U. Ogunka-Nnoka
Keyword(s):  
Oxidative Stress ◽  
Negative Control ◽  
Control Group ◽  
Albino Rats ◽  
Root Extract ◽  
Annona Muricata ◽  
Bioactive Components ◽  
Crude Fibre ◽  
Ethanol Extracts ◽  
Wistar Albino Rats

The study was designed to determine the nutrient, bioactive components and the effects of ethanol extracts of the leaves of Annona muricata (AM) and the roots of Fagara zanthoxyloide (FZ) on zidovudine-induced oxidative stress in wistar albino rats. Wistar albino rats were divided into four groups of five rats each. Groups 2-4 were induced with 100 g/ml/Kg bw of zidovudine (ZDV) and varying concentrations of the extracts (group 3 and 4); while group 1 served as the control. The results of the proximate composition of both plants showed the following ranges: moisture (10.32-18.30%), ash (0.65-9.45%), crude protein (1.38-10.54%), crude fat (2.35-9.73%), crude fibre (3.00-15.53%) and carbohydrate (50.19-65.23%). Iron was the highest mineral present in all the samples followed by zinc and calcium for FZ and AM respectively; while folate and ascorbic acid were the highest vitamins present in both samples. Phytochemical composition results revealed higher concentrations of alkaloids, flavonoid and phenols in the leaves and roots of both samples. Acute toxicity study revealed no short term toxicity below 6 g/ml/Kg bw for the leave extract of Annona muricata and 4 g/ml/Kg bw for the root extract of Fagara zanthoxyloide. Administration of zidovudine to albino rats resulted in a significant increase (p≤0.05) in biomarkers of oxidative stress; while subsequent treatment with ethanol extracts of the leaves of AM and roots of FZ reduced the activities of superoxide dismutase, catalase and glutathione. The splenic histology revealed atrophy, early onset necrosis and reduction in sinusoidal pore size in the negative control group which were absent in the extract treatment groups indicating a protective effect conferred by extracts against oxidative stress. The study, therefore suggests that these plants may play some key roles in alleviating salient nutritional, physiological and oxidative stress related challenges.

Effect of Propolis-Supplemented Diet on Body Composition and Endocrine Function of Adipose Tissue

2020 ◽  
Vol 19 (2) ◽  
pp. 217-221
Author(s):  
Maria Jesús Lisbona-González ◽  
Candela Reyes-Botella ◽  
Esther Muñoz-Soto ◽  
Maria Victoria Olmedo-Gaya, ◽  
Jorge Moreno-Fernandez ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Composition ◽  
Adipose Tissue ◽  
Endocrine Function ◽  
Control Group ◽  
Albino Rats ◽  
Standard Diet ◽  
Reduced Body ◽  
Esterified Fatty Acids ◽  
Wistar Albino Rats

Adipose tissue is an endocrine organ and has central role in interaction with other organs or tissues while propolis can induce lipolysis. Therefore, the aim of this study is to provide detailed information about adipose tissue homeostasis modifications and body composition during propolis supplement consumption. Twenty male Wistar albino rats (8 weeks) were divided into two groups of 10 animals each and fed for 90 days with two different types of diets: standard for the control group (diet C) and standard diet + 2% propolis (diet P). Thyroid hormones did not show differences, while ghrelin and adiponectin decreased in the group that was fed propolis. Insulin, leptin, and non-esterified fatty acids also increased along with reduced body weight and fat, in addition to increased lean mass when propolis was in the diet. We conclude that propolis could decrease ghrelin and adiponectin but increase non-esterified fatty acids and insulin secretion, which improves body composition.

scholarly journals The Antioxidant Effect of Curcumin and Rutin on Oxidative Stress Biomarkers in Experimentally Induced Periodontitis in Hyperglycemic Wistar Rats

Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1332
Author(s):  
Gilda M. Iova ◽  
Horia Calniceanu ◽  
Adelina Popa ◽  
Camelia A. Szuhanek ◽  
Olivia Marcu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Diabetic Rats ◽  
Gingival Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Significant Difference ◽  
The Impact ◽  
Experimentally Induced

Background: There is a growing interest in the correlation between antioxidants and periodontal disease. In this study, we aimed to investigate the effect of oxidative stress and the impact of two antioxidants, curcumin and rutin, respectively, in the etiopathology of experimentally induced periodontitis in diabetic rats. Methods: Fifty Wistar albino rats were randomly divided into five groups and were induced with diabetes mellitus and periodontitis: (1) (CONTROL)—control group, (2) (DPP)—experimentally induced diabetes mellitus and periodontitis, (3) (DPC)—experimentally induced diabetes mellitus and periodontitis treated with curcumin (C), (4) (DPR)—experimentally induced diabetes mellitus and periodontitis treated with rutin (R) and (5) (DPCR)—experimentally induced diabetes mellitus and periodontitis treated with C and R. We evaluated malondialdehyde (MDA) as a biomarker of oxidative stress and reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG and catalase (CAT) as biomarkers of the antioxidant capacity in blood harvested from the animals we tested. The MDA levels and CAT activities were also evaluated in the gingival tissue. Results: The control group effect was statistically significantly different from any other groups, regardless of whether or not the treatment was applied. There was also a significant difference between the untreated group and the three treatment groups for variables MDA, GSH, GSSG, GSH/GSSG and CAT. There was no significant difference in the mean effect for the MDA, GSH, GSSG, GSH/GSSG and CAT variables in the treated groups of rats with curcumin, rutin and the combination of curcumin and rutin. Conclusions: The oral administration of curcumin and rutin, single or combined, could reduce the oxidative stress and enhance the antioxidant status in hyperglycemic periodontitis rats.

Role of TLR-4/IL-6/TNF-α, COX-II and eNOS/iNOS pathways in the impact of carvedilol against hepatic ischemia reperfusion injury

2021 ◽  
pp. 096032712199944
Author(s):  
Mohamed IA Hassan ◽  
Fares EM Ali ◽  
Abdel-Gawad S Shalkami
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Liver Enzymes ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Aim: Hepatic ischemia/reperfusion (I/R) injury is a syndrome involved in allograft dysfunction. This work aimed to elucidate carvedilol (CAR) role in hepatic I/R injury. Methods: Male rats were allocated to Sham group, CAR group, I/R group and CAR plus I/R group. Rats subjected to hepatic ischemia for 30 minutes then reperfused for 60 minutes. Oxidative stress markers, inflammatory cytokines and nitric oxide synthases were measured in hepatic tissues. Results: Hepatocyte injury following I/R was confirmed by a marked increase in liver enzymes. Also, hepatic I/R increased the contents of malondialdehyde however decreased glutathione contents and activities of antioxidant enzymes. Furthermore, hepatic I/R caused elevation of toll-like receptor-4 (TLR-4) expression and inflammatory mediators levels such as tumor necrosis factor-α, interleukin-6 and cyclooxygenase-II. Hepatic I/R caused down-regulation of endothelial nitric oxide synthase and upregulation of inducible nitric oxide synthase expressions. CAR treatment before hepatic I/R resulted in the restoration of liver enzymes. Administration of CAR caused a significant correction of oxidative stress and inflammation markers as well as modulates the expression of endothelial and inducible nitric oxide synthase. Conclusions: CAR protects liver from I/R injury through reduction of the oxidative stress and inflammation, and modulates endothelial and inducible nitric oxide synthase expressions.

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