Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

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.

The protective and therapeutic effects of linalool against doxorubicin-induced cardiotoxicity in Wistar albino rats

2019 ◽  
Vol 38 (7) ◽  
pp. 803-813 ◽  
Author(s):  
Z Oner ◽  
E Altınoz ◽  
H Elbe ◽  
N Ekinci
Keyword(s):  
Caspase 3 ◽  
Inflammatory Cell ◽  
Cardiac Tissue ◽  
Saline Solution ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Treatment Groups ◽  
Wistar Albino Rats ◽  
Plasma Creatine Kinase

The aim of the present study was to determine the protective and therapeutic effects of linalool (LIN) against doxorubicin (DOX)-induced cardiotoxicity in rats histologically and biochemically. In experiments, 64 male Wistar albino rats were randomly divided into eight groups ( n = 8). These groups were control (C) (0.9% saline solution), DOX (20 mg/kg DOX), LIN50 (50 mg/kg LIN), LIN100 (100 mg/kg LIN), DOX + LIN50 (20 mg/kg DOX and 50 mg/kg LIN), DOX + LIN100 (20 mg/kg DOX and 100 mg/kg LIN), LIN50 + DOX (50 mg/kg LIN and 20 mg/kg DOX), and LIN100 + DOX (100 mg/kg LIN and 20 mg/kg DOX). It was determined that necrosis and extensive inflammatory cell infiltration were observed in the DOX group. It was determined that histopathological changes significantly decreased in groups treated with LIN after DOX administration. While the caspase-3 immunostaining was highly evident in DOX group apoptotic cells ( p < 0.001, for all), the intensity of caspase-3 immunostaining in the treatment groups decreased ( p < 0.05). While DOX administration resulted in a significant increase in malondialdehyde (MDA) levels and plasma Creatine kinase (CK) and lactate dehydrogenase (LDH) levels in cardiac tissue when compared to the C groups, it was observed that DOX + LIN administration led to a significant decrease in MDA, plasma CK and LDH levels and a significant increase in glutathione (GSH), superoxide dismutase, and catalase enzyme levels. Finally, it was concluded that DOX led to heavy cardiotoxicity and DOX + LIN administration could remove cardiomyopathy symptoms.

Cadmium acts as a silent killer of liver by inducing oxidative stress and hepatocellular injury and a possible amelioration by vitamin B12 and folic acid in rat model

2019 ◽  
Vol 1 ◽  
pp. 105-117
Author(s):  
A. Banerjee ◽  
P. Nandi ◽  
C. Bhattacharya ◽  
Z. Kabir ◽  
S. Mukherjee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Rat Model ◽  
Male Rats ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Hepatocellular Injury ◽  
Male Adult ◽  
Wistar Albino Rats

<br/><b>Purpose:</b> To investigate the involvement of oxidative stress in Cadmium (Cd) induced alteration in the functional status of the liver. And to assess the efficacy of folic acid and vitamin B12 in preventing Cd-induced damage in the same. <br/><b>Materials and methods:</b> The experiment was carried out for four weeks. For the experiment, 25 healthy male adult Wistar albino rats were randomly selected and were divided into five equal groups and treated as control, treated with Cd, supplemented with vitamin B12 and folic acid and in the combination of these two. After 28 days the liver function enzymes and oxidative stress parameters were measured. <br/><b>Results:</b> Cd is the silent killer of the hepatic system through the induction of oxidative stress in male rats. From this investigation, it is evident that the folic acid+vitamin B12 possess significant hepatoprotective and antioxidant activity against Cd-induced hepatotoxicity in the rat model. In addition, results revealed that the folic acid alone and or in combination with vitamin B12 blunted the hepatotoxic effect significantly. <br/><b>Conclusions:</b> Based on results obtained, it can be concluded that folic acid and vitamin B12 offer a protective effect in Cd-induced oxidative stress associated with hepatocellular injury. Folic acid and vitamin B12 can be considered as a potent natural antioxidant which has the capacity to provide protection against Cd-induced oxidative stress in the liver in rats. However, to elucidate the exact mechanism of this modulatory effect and to examine its potential therapeutic effects further studies are essential.

scholarly journals Manganese-Induced Nephrotoxicity Is Mediated through Oxidative Stress and Mitochondrial Impairment

2020 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Amir Mohammad Niknahad ◽  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Leila Moezi ◽  
Reza Heidari
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Essential Element ◽  
The Other ◽  
Tubular Atrophy ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity

Manganese (Mn) is an essential element that is incorporated in various metabolic pathways and enzyme structures. On the other hand, a range of adverse effects has been described in association with Mn overexposure. Mn is a well-known neurotoxic agent in mammals. Renal injury is another adverse effect associated with Mn intoxication. No precise mechanism for Mn nephrotoxicity has been identified so far. The current study was designed to evaluate the potential mechanisms of Mn-induced renal injury. Rats were treated with Mn (20 and 40 mg/mL, respectively, in drinking water) for 30 consecutive days. Markers of oxidative stress, as well as several mitochondrial indices, were assessed in the kidney tissue. Renal injury was evident in Mn-treated animals, as judged by a significant increase in serum BUN and creatinine. Moreover, urinalysis revealed a significant increase in urine glucose, phosphate, and protein in Mn-treated rats. Kidney histopathological alterations, including tubular atrophy, interstitial inflammation, and necrosis, were also detected in Mn-treated animals. Biomarkers of oxidative stress, including an increment in reactive oxygen species (ROS), lipid peroxidation, and oxidized glutathione (GSSG), were detected in Mn-treated groups. On the other hand, kidney glutathione (GSH) stores and total antioxidant capacity were depleted in Mn groups. Mn exposure was associated with significant mitochondrial depolarization, decreased mitochondrial dehydrogenases activity, mitochondrial permeabilization, and depletion of adenosine tri-phosphate (ATP) content. These data highlight oxidative stress and mitochondrial impairment as potential mechanisms involved in Mn-induced renal injury.

scholarly journals Bisphenol-A induced oxidative stress, inflammatory gene expression, and metabolic and histopathological changes in male Wistar albino rats: protective role of boron

2019 ◽  
Vol 8 (2) ◽  
pp. 262-269 ◽  
Author(s):  
Ulas Acaroz ◽  
Sinan Ince ◽  
Damla Arslan-Acaroz ◽  
Zeki Gurler ◽  
Hasan Huseyin Demirel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Bisphenol A ◽  
Protective Role ◽  
Albino Rats ◽  
Histopathological Changes ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Wistar Albino Rats

Boron reversed Bisphenol-A induced alterations.

The Effect of Resveratrol on Neurodegenerative Disorders: Possible Protective Actions Against Autophagy, Apoptosis, Inflammation and Oxidative Stress

2019 ◽  
Vol 25 (19) ◽  
pp. 2178-2191 ◽  
Author(s):  
Mohammad H. Pourhanifeh ◽  
Rana Shafabakhsh ◽  
Russel J. Reiter ◽  
Zatollah Asemi
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorders ◽  
Cell Damage ◽  
Current Evidence ◽  
Therapeutic Effects ◽  
Neuronal Function ◽  
Beneficial Effects ◽  
Cellular Processes ◽  
And Oxidative Stress

The prevalence of neurodegenerative disorders characterized by the loss of neuronal function is rapidly increasing. The pathogenesis of the majority of these diseases is not entirely clear, but current evidence has shown the possibility that autophagy, apoptosis, inflammation and oxidative stress are involved. The present review summarizes the therapeutic effects of resveratrol on neurodegenerative disorders, based on the especially molecular biology of these diseases. The PubMed, Cochrane, Web of Science and Scopus databases were searched for studies published in English until March 30th, 2019 that contained data for the role of inflammation, oxidative stress, angiogenesis and apoptosis in the neurodegenerative disorders. There are also studies documenting the role of molecular processes in the progression of central nervous system diseases. Based on current evidence, resveratrol has potential properties that may reduce cell damage due to inflammation. This polyphenol affects cellular processes, including autophagy and the apoptosis cascade under stressful conditions. Current evidence supports the beneficial effects of resveratrol on the therapy of neurodegenerative disorders.

Can ursolic acid be beneficial against diabetes in rats?

2018 ◽  
Vol 43 (5) ◽  
pp. 520-529 ◽  
Author(s):  
Merve Bacanlı ◽  
Sevtap Aydın ◽  
Hatice Gül Anlar ◽  
Tuğbagül Çal ◽  
Nuray Arı ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Profile ◽  
Ursolic Acid ◽  
Albino Rats ◽  
Antioxidant Enzyme Activities ◽  
Hepatic Enzyme ◽  
Beneficial Effects ◽  
Oxidative Stress Parameters ◽  
Wistar Albino Rats ◽  
Stress Parameters

Abstract Objective: Diabetes mellitus, a heteregenous metabolic and chronic disease, is a growing health problem especially in developing countries. It is claimed that diabetes associated with increased formation of free radicals and decrease in antioxidant potential and also alterations in lipid profile and enzyme levels. Ursolic acid is commonly used in traditional Chinese medicine due to its beneficial effects. The aim of this study was to investigate the effects of ursolic acid on streptozotocin-induced diabetes in Wistar albino rats. Methods: DNA damage was evaluated in the blood and liver cells of rats by alkaline comet assay. The activities of antioxidant enzymes, oxidative stress parameters, biochemical parameters, hepatic enzyme levels and lipid profile parameters were also evaluated. Results: The results of this study demonstrate that diabetes caused genotoxic damage, changes in hepatic enzyme and lipid profile, biochemical and antioxidant enzyme activities and oxidative stress parameters in rats. Ursolic acid was found to be protective against diabetes induced effects in blood and liver samples of rats. Conclusions: According to our results, it seems that ursolic acid may be beneficial against diabetes and its adverse effects in rats.

scholarly journals Biochemical Changes Followed Experimental Respiratory Distress by Benzene Vapours

2019 ◽  
Vol 12 (1) ◽  
pp. 403-409
Author(s):  
Abdel Maksoud H. A. ◽  
Mahfouz M. K. ◽  
Omnia M. A. ◽  
Abdullah M. H ◽  
Eltabey M. E. ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Respiratory Distress ◽  
Biochemical Parameters ◽  
Albino Rats ◽  
Histopathological Changes ◽  
Oxidative Stress Parameters ◽  
And Oxidative Stress ◽  
Alveolar Septa ◽  
Stress Parameters

Monitoring of exposure to chemical matters is seriously needed for evaluating health hazards resulted from its inhalation. The present study was carried out to determine the biochemical, immunological and oxidative stress parameters as well as the possible histological effects of exposure to benzene vapours in male albino rats. Results indicated that; Benzene vapours exposure induced significant increasing in Myeloperoxidase (MPO) enzyme levels. This goes with marked immunologic changes presented by decreases in immunoglobulins; IgA and IgG, along with increases in levels of IgM and IgE. Also, Malondialdehyde (MDA) levels were significantly increased. Meanwhile, reduction in different biochemical parameters including; Superoxide Dismutase (SOD), Catalase (CAT) levels and Glutathione (GSH) content. Lung sections taken showed; Thickening of alveolar septa with chronic inflammation and /or fibrosis, Congested vessels/thick walled vessels and Peri-bronchiolar fibrosis. Hence, the study concluded that; prolonged benzene (BNZ) vapours exposure lead to biochemical, immune disterbance and histopathological changes probably through potentiating oxidative stress and inflammation pathways.

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