scholarly journals Evaluation of the Protective Effects of Hydroalcoholic Extract of Satureja avromanica Against Malathion-induced Oxidative Stress in the Liver: An Experimental Study

2020 ◽  
Author(s):  
Akram Ranjbar ◽  
Negar Mehri ◽  
Hassan Ghasemi ◽  
Dara Dastan ◽  
Farzaneh Kazemi Najafabadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Tissue ◽  
Organophosphorus Pesticides ◽  
Treated Group ◽  
Protective Effects ◽  
Stress Injury ◽  
Hydroalcoholic Extract ◽  
Total Antioxidant ◽  
Satureja Avromanica ◽  
Harmful Effects

Background: Studies have shown that organophosphorus pesticides such as malathion induces oxidative stress injury and tissue damage. Objectives: This research aimed to determine the effects of the hydroalcoholic extracts of Satureja Avromanica (SA) on the liver function of malathion-poisoned animals. Methods: Twenty-eight rats were divided into four groups of the control, SA (20 mg/kg), malathion+SA, and malathion. Animals received malathion 150 mg/kg and SA 20 mg/kg for one week through intraperitoneal injection. Then, their liver and blood samples were extracted, and alanine aminotransferase, aspartate aminotransferase concentrations in serum as well as biomarkers of oxidative stress such as Lipid Peroxidation (LPO), Total Antioxidant Capacity (TAC) and Total Thiol Groups (TTG) in the liver tissue were measured. Results: The results showed that the SA administration reduced the level of liver LPO compared with that in the malathion group. Also, receiving SA increased liver TAC and TTG levels in rats, which this difference was significant compared with the malathion group. Besides, the SA group showed a significant decrease in liver enzyme levels, compared with the malathion-treated group. Conclusion: According to the results, SA exerted protective effects against malathion poisoning, through reduction of oxidative stress. Therefore, SA may be an antioxidant to counteract the harmful effects of malathion poising in liver tissue.

Chelating effects of carnosine in ameliorating nickel-induced nephrotoxicity in rats

2017 ◽  
Vol 95 (12) ◽  
pp. 1426-1432 ◽  
Author(s):  
Parisa Hasanein ◽  
Zhila Felegari
Keyword(s):  
Oxidative Stress ◽  
Reduced Glutathione ◽  
Therapeutic Option ◽  
Treated Group ◽  
Renal Tissue ◽  
Protective Effects ◽  
Nickel Toxicity ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Biochemical Abnormalities

The kidney is one of the main organs affected by nickel toxicity. We investigated the protective effects of carnosine on nickel-induced oxidative stress in kidney of rats. Animals received NiSO4 (20 mg·kg−1·day−1 intragastrically) and (or) carnosine (10 mg·kg−1·day−1 intragastrically) for 21 days and then were evaluated for biochemical, molecular, and histopathological alterations. Nickel caused an increase in renal levels of malondialdehyde and a decrease in reduced glutathione, catalase, and superoxide dismutase levels and total antioxidant capacity. Carnosine prevented the prooxidant and antioxidant imbalance induced by nickel. Nickel-treated rats showed an increase in serum creatinine, urea, and uric acid with a concomitant decrease in albumin. Nickel markedly accumulated in kidney of exposed rats, but its concentration was effectively reduced by carnosine treatment. Carnosine corrected the biochemical abnormalities and the elevated renal TNF-α and IL-6 levels in the nickel-treated group. It also attenuated nickel-induced abnormalities in renal architecture. Although carnosine showed antioxidant and anti-inflammatory effects in renal tissue of nickel-exposed rats, we cannot clearly attribute the protective effect of carnosine to these effects. Instead, the beneficial effect of carnosine observed in the current study may be due to chelation between nickel and carnosine. Thus, carnosine may represent a therapeutic option to protect against nickel-induced nephrotoxicity that deserves further consideration and examination.

scholarly journals Alleviation of Oxidative Stress in Dental Pulp Cells Following 4-Hexylresorcinol Administration in a Rat Model

2021 ◽  
Vol 11 (8) ◽  
pp. 3637
Author(s):  
Jun-Ho Chang ◽  
Dae-Won Kim ◽  
Seong-Gon Kim ◽  
Tae-Woo Kim
Keyword(s):  
Oxidative Stress ◽  
Dental Pulp ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Mandibular Incisor ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Pulp Cells ◽  
Pre Treatment

Damaged dental pulp undergoes oxidative stress and 4-hexylresorcinol (4HR) is a well-known antioxidant. In this study, we aimed to evaluate the therapeutic effects of a 4HR ointment on damaged dental pulp. Pulp cells from rat mandibular incisor were cultured and treated with 4HR or resveratrol (1–100 μM). These treatments (10–100 μM) exerted a protective effect during subsequent hydrogen peroxide treatments. The total antioxidant capacity and glutathione peroxidase activity were significantly increased following 4HR or resveratrol treatment (p < 0.05), while the expression levels of TNF-α and IL1β were decreased following the exposure to 4HR pre-treatment in an in vitro model. Additionally, the application of 4HR ointment in an exposed dental pulp model significantly reduced the expression of TNF-α and IL1β (p < 0.05). Conclusively, 4HR exerted protective effects against oxidative stress in dental pulp tissues through downregulating TNF-α and IL1β.

scholarly journals Remote post-conditioning and allopurinol reduce ischemia-reperfusion injury in an infra-renal ischemia model

2018 ◽  
Vol 12 (12) ◽  
pp. 341-349 ◽  
Author(s):  
Rafael Inácio Brandão ◽  
Ricardo Zanetti Gomes ◽  
Luana Lopes ◽  
Filipe Silva Linhares ◽  
José Carlos Rebuglio Vellosa ◽  
...  
Keyword(s):  
Histological Analysis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemia And Reperfusion ◽  
Protective Effects ◽  
Positive Effects ◽  
Additional Protection ◽  
Total Antioxidant ◽  
Lactate Levels ◽  
Harmful Effects

Background: The aim of this study was to evaluate the effects of the antioxidant allopurinol and ischemic post-conditioning on the deleterious effects of ischemia followed by reperfusion (I/R) in a standardized model of ischemia involving infra-renal aortic occlusion in rats. Methods: The animals were randomly divided into five groups: (A) animals not subjected to ischemia; (B) animals subjected to 2 h of ischemia and reperfusion only once; (C) animals given an allopurinol dose by gavage, then subjected to 2 h of ischemia and reperfusion only once; (D) animals subjected to 2 h of ischemia and post-conditioning and (E) animals that received allopurinol, then subjected to 2 h of ischemia and post-conditioning. The blood samples and small intestine segments were harvested for analysis after 3 days. Results: The protective effects of the use of allopurinol and ischemic post-conditioning were observed by measuring aspartate aminotransferase, alanine aminotransferase and lactate levels. The benefits of post-conditioning were evident from the total antioxidant capacity and creatinine levels, but these could not ascertain any positive effects of allopurinol. The histological analysis of mesentery revealed that both methods were effective in minimizing the harmful effects of the ischemia and reperfusion process. Conclusion: Individual protocols significantly reduced I/R systemic injuries, but no additional protection was observed when the two strategies were combined.

scholarly journals The role of nitrosative and oxidative stress in rainbow trout (Oncorhynchus mykiss) liver tissue applied mercury chloride (HgCl2)

2021 ◽  
Vol 38 (3) ◽  
pp. 269-273
Author(s):  
Mehmet Reşit Taysı ◽  
Muammer Kırıcı ◽  
Mahinur Kırıcı ◽  
Hasan Ulusal ◽  
Bünyamin Söğüt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Liver Tissue ◽  
Stress Index ◽  
Mercury Chloride ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Total Antioxidant ◽  
Ld50 Value

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P<0.05), however, this difference was not significant (P>0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

Abstract 352: Real-time Intravital Optical Imaging Reflects the Dynamic Changes of Oxidative Stress Induced by Cigarette Smoking in Vasculatures

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Ji Bak Kim ◽  
Jiheun Ryu ◽  
Joon Woo Song ◽  
Dong Joo Oh ◽  
DaeGab Gweon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoking ◽  
Optical Imaging ◽  
Real Time ◽  
Treated Group ◽  
Fluorescence Signal ◽  
Ros Production ◽  
Protective Effects ◽  
Dynamic Changes

Background: Reactive oxygen species (ROS) play a central role in cigarette smoking-induced atherogenesis. The present study aims to assess the smoking-induced acute oxidative stress within vasculatures, and evaluates whether the resveratrol, a natural polyphenol antioxidant, can counteract this ROS production, using a customized, high resolution intravital optical imaging in real-time. Methods and Results: 20-week-old male C57BL/6 mice were divided into four groups according to the preceding administration of resveratrol (R) (25mg/kg via gavage, for 7 days) and exposure to cigarette smoke (CS). To in vivo assess acute oxidative stress in blood vessels, dihydroethidium, which forms a red fluorescence (ethidium, excitation/emission: 520nm/610nm) upon reaction with ROS, was injected intraperitoneally. During CS exposure, temporal changes of fluorescence signals from the mouse cremaster muscle including vasculatures were assessed by intravital optical imaging for 15 minutes. Fluorescence signals were much more pronounced in CS exposed mice than controls (p<0.001). Resveratrol p.o. significantly reduced the CS-induced ROS signals compared to the non-treated group (fluorescence signal to noise ratio, SNR, 2.51±0.09 vs. 12.52±2.116, p=0.0002) (Figure A). Without CS exposure, fluorescence signals in targeted vasculatures were very low showing no difference between groups (SNR, 1.65±0.19 vs. 1.53±0.07, p=0.80) (Figure A). Lipid peroxidation was increased in CS group and significantly attenuated in resveratrol-treated mice (Figure B). Fluorescence microscopy and immunostainings corroborated the in vivo findings. Conclusions: The intravital optical imaging was able to in vivo estimate the dynamic changes of ROS production by CS exposure. Our data demonstrated that even a brief exposure to CS increased oxidative stress in vasculatures promptly, and the resveratrol exerts protective effects against the CS-induced acute oxidative stress.

Protective effects of deferoxamine on lead-induced cardiotoxicity in rats

2020 ◽  
Vol 36 (10) ◽  
pp. 800-806
Author(s):  
Alireza Gazeri ◽  
Azadeh Aminzadeh
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Chelating Agent ◽  
Industrial Applications ◽  
Protective Effects ◽  
Industrialized Countries ◽  
Protective Capacity ◽  
Cardiac Tissues ◽  
Stress Markers ◽  
Total Antioxidant

Because of the numerous industrial applications of lead (Pb), Pb poisoning is an important public health threat in the world particularly in developing and industrialized countries. Oxidative stress is one of the important mechanisms of Pb-mediated toxicity. Deferoxamine (DFO) is an iron chelating agent that has recently shown antioxidant and antiapoptotic effects. This study investigated the protective capacity of DFO against Pb-induced cardiotoxicity in rats. We used five groups in this study: control, DFO (300 mg/kg), Pb (50 mg/kg), DFO (150 mg/kg) + Pb, DFO (300 mg/kg) + Pb. DFO was administered intraperitoneally 30 min before intraperitoneal injection of Pb for 5 days. After drug treatment, the levels of lactate dehydrogenase (LDH), lipid peroxidation (LPO), glutathione (GSH), and antioxidant enzymes were measured in serum and heart samples. The results showed that pretreatment with DFO reduced Pb-induced oxidative stress markers in serum and cardiac tissues. We found that LDH and LPO levels were significantly increased in Pb-treated rats and decreased with DFO pre-administration. Furthermore, the decreased activities of total antioxidant capacity, and GSH were observed after Pb treatment. However, DFO administration effectively prevented the Pb-induced alterations of these antioxidant enzymes activities. In conclusion, the results presented here indicate that DFO has protective effects in Pb-induced cardiotoxicity in rats, probably due to its antioxidant action and inhibition of oxidative stress.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

scholarly journals Isoliquiritigenin Ameliorates Acute Pancreatitis in Mice via Inhibition of Oxidative Stress and Modulation of the Nrf2/HO-1 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Xinnong Liu ◽  
Qingtian Zhu ◽  
Min Zhang ◽  
Tao Yin ◽  
Rong Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Pancreatitis ◽  
Tissue Injury ◽  
Pancreatic Tissue ◽  
Zinc Protoporphyrin ◽  
Dependent Manner ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Flavonoid Monomer

Oxidative stress plays a crucial role in the pathogenesis of acute pancreatitis (AP). Isoliquiritigenin (ISL) is a flavonoid monomer with confirmed antioxidant activity. However, the specific effects of ISL on AP have not been determined. In this study, we aimed to investigate the protective effect of ISL on AP using two mouse models. In the caerulein-induced mild acute pancreatitis (MAP) model, dynamic changes in oxidative stress injury of the pancreatic tissue were observed after AP onset. We found that ISL administration reduced serum amylase and lipase levels and alleviated the histopathological manifestations of pancreatic tissue in a dose-dependent manner. Meanwhile, ISL decreased the oxidative stress injury and increased the protein expression of the Nrf2/HO-1 pathway. In addition, after administering a Nrf2 inhibitor (ML385) or HO-1 inhibitor (zinc protoporphyrin) to block the Nrf2/HO-1 pathway, we failed to observe the protective effects of ISL on AP in mice. Furthermore, we found that ISL mitigated the severity of pancreatic tissue injury and pancreatitis-associated lung injury in a severe acute pancreatitis model induced by L-arginine. Taken together, our data for the first time confirmed the protective effects of ISL on AP in mice via inhibition of oxidative stress and modulation of the Nrf2/HO-1 pathway.

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