An investigation of the effect of thiamine pyrophosphate on cisplatin-induced oxidative stress and DNA damage in rat brain tissue compared with thiamine

This study investigated the effects of thiamine pyrophosphate (TPP) at dosages of 10 and 20 mg/kg on oxidative stress induced in rat brain tissue with cisplatin and compared this with thiamine. Cisplatin neurotoxicity represents one of the main restrictions on the drug being given in effective doses. Oxidative stress is considered responsible for cisplatin toxicity. Our results showed that cisplatin increased the levels of oxidant parameters such as lipid peroxidation (thio barbituric acid reactive substance (TBARS)) and myeloperoxidase (MPO) in brain tissue and suppressed the effects of antioxidants such as total glutathione (GSH) and superoxide dismutase (SOD). TPP, especially at a dosage of 20 mg/kg, significantly reduced TBARS and MPO levels that increase with cisplatin administration compared with the thiamine group, while TPP significantly increases GSH and SOD levels. In addition, the level of 8-Gua (guanine), a product of DNA damage, was 1.7 ± 0.12 8-hydroxyl guanine (8-OH Gua)/105 Gua in brain tissue in the control group receiving cisplatin, compared with 0.97 ± 0.03 8-OH Gua/105 Gua in the thiamine pyrophosphate (20 mg/kg) group and 1.55 ± 0.11 8-OH Gua/105 Gua in the thiamine (20 mg/kg) group. These results show that thiamine pyrophosphate significantly prevents oxidative damage induced by cisplatin in brain tissue, while the protective effect of thiamine is insignificant.

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Mammalian Target of Rapamycin (mTOR) Inhibitor Improves Local Immune Microenvironment and Reduces Seizures via Increasing miR-211 Level in Rat Brain

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2022.2968 ◽

2022 ◽

Vol 12 (4) ◽

pp. 841-847

Author(s):

Meijiao Du ◽

Zhengmei Wang ◽

Geng Su ◽

Yunxia Zhou ◽

Chuan Luo

Keyword(s):

Rat Brain ◽

Brain Tissue ◽

Mtor Inhibitor ◽

Symptom Relief ◽

Mtor Inhibitors ◽

Inflammatory Factors ◽

Control Group ◽

Tunel Staining ◽

Immune Microenvironment ◽

Rat Brain Tissue

This study aims to analyze the role of mTOR inhibitor on the expression of miR-211 in rat brain tissue and the biological effect of miR-211 in attenuating seizure. Rats were randomly divided into four groups, and the number of seizures and the duration of single seizure were observed within 24 hours after intervention. The level of miR-211 in brain tissue was detected by RT qPCR, the apoptosis of nerve cells was assessed by TUNEL staining, the level of immune cells was detected by flow cytometry, and the level of serum inflammatory factors was determined by ELISA. The number of seizures and the duration of single seizure in the three groups treated by rapamycin within 24 hours were lower than those in the control group, and the symptom relief in group C was the best. After treatment, the expression level of miR-211 in the brain tissue of epileptic rats increased. TUNEL staining showed that neuronal apoptosis was obvious in epileptic rats. The anti apoptotic ability of group C was the most significant, followed by group D and group B. Compared with group A, the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells in brain tissue of group C were decreased, while the levels of IL-2 and IFN-γ were lower in group C than those in control. In group C (n = 5), the levels of CD3+ cells, CD8+ cells and CD4+/CD25+ cells were elevated, and the levels of immune related cytokines IL-2 and IFN-γ were higher than those of rats without miR-211 inhibition. mTOR inhibitors can improve the local immune microenvironment, reduce the release of inflammatory factors, and finally decrease the frequency and duration of seizures by up regulating the level of miR-211 in rat brain tissue.

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Oxidative stress induced by the Fe2+/ascorbic acid system or model ischemia in vitro: effect of carvedilol and pyridoindole antioxidant SMe1EC2 in young and adult rat brain tissue

Interdisciplinary Toxicology ◽

10.2478/v10102-010-0051-x ◽

2010 ◽

Vol 3 (4) ◽

pp. 122-126 ◽

Cited By ~ 9

Author(s):

Zdenka Gáspárová ◽

Oľga Ondrejičková ◽

Alena Gajdošíková ◽

Andrej Gajdošík ◽

Vladimír Šnirc ◽

...

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Rat Brain ◽

Brain Tissue ◽

Protein Carbonyl ◽

Experimental Models ◽

Adult Rat ◽

Adult Rat Brain ◽

Rat Brain Tissue

Oxidative stress induced by the Fe2+/ascorbic acid system or model ischemiain vitro: effect of carvedilol and pyridoindole antioxidant SMe1EC2 in young and adult rat brain tissueNew effective strategies and new highly effective neuroprotective agents are being searched for the therapy of human stroke and cerebral ischemia. The compound SMe1EC2 is a new derivative of stobadine, with enhanced antioxidant properties compared to the maternal drug. Carvedilol, a non-selective beta-blocker, possesses besides its cardioprotective and vasculoprotective properties also an antioxidant effect. We compared the effect of carvedilol and SMe1EC2, antioxidants with a similar chemical structure, in two experimental models of oxidative stress in young and adult rat brain tissue. SMe1EC2 was found to improve the resistance of hippocampal neurons to ischemiain vitroin young and even in 18-month-old rats and inhibited formation of protein carbonyl groups induced by the Fe2+/ascorbic acid pro-oxidative system in brain cortex homogenates of young rats. Carvedilol exerted a protective effect only in the hippocampus of 2-month-old rats and that at the concentration 10-times higher than did SMe1EC2. The inhibitory effect of carvedilol on protein carbonyl formation induced by the pro-oxidative system was not proved in the cortex of either young or adult rats. An increased baseline level of the content of protein carbonyl groups in the adult versus young rat brain cortex confirmed age-related changes in neuronal tissue and may be due to increased production of reactive oxygen species and low antioxidant defense mechanisms in the adult rat brain. The results revealed the new pyridoindole SMe1EC2 to be more effective than carvedilol in neuroprotection of rat brain tissue in both experimental models involving oxidative stress.

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Ganoderma Lucidum Protects Rat Brain Tissue Against Trauma-Induced Oxidative Stress

Korean Journal of Neurotrauma ◽

10.13004/kjnt.2017.13.2.76 ◽

2017 ◽

Vol 13 (2) ◽

pp. 76 ◽

Cited By ~ 3

Author(s):

Özevren Hüseyin ◽

İrtegün Sevgi ◽

Deveci Engin ◽

Aşır Fırat ◽

Pektanç Gülsüm ◽

...

Keyword(s):

Oxidative Stress ◽

Rat Brain ◽

Brain Tissue ◽

Ganoderma Lucidum ◽

Rat Brain Tissue

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Carnosine supplementation protects rat brain tissue against ethanol-induced oxidative stress

Molecular and Cellular Biochemistry ◽

10.1007/s11010-009-0369-x ◽

2010 ◽

Vol 339 (1-2) ◽

pp. 55-61 ◽

Cited By ~ 14

Author(s):

Ummuhani Ozel Turkcu ◽

Ayşe Bilgihan ◽

Gursel Biberoglu ◽

Oznur Mertoglu Caglar

Keyword(s):

Oxidative Stress ◽

Rat Brain ◽

Brain Tissue ◽

Rat Brain Tissue

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Protective Effect of Melatonin on the Oxidative Stress Caused by Diabetes and Forced Swimming Exercise on Rat Brain Tissue

Turkiye Klinikleri Journal of Medical Sciences ◽

10.5336/medsci.2011-27367 ◽

2012 ◽

Vol 32 (3) ◽

pp. 782-787 ◽

Cited By ~ 1

Author(s):

Mürsel Bi ÇER

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Rat Brain ◽

Brain Tissue ◽

Forced Swimming ◽

Swimming Exercise ◽

Rat Brain Tissue

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Manganese leads to an increase in markers of oxidative stress as well as to a shift in the ratio of Fe(ii)/(iii) in rat brain tissue

Metallomics ◽

10.1039/c4mt00022f ◽

2014 ◽

Vol 6 (4) ◽

pp. 921 ◽

Cited By ~ 56

Author(s):

Katharina Fernsebner ◽

Julia Zorn ◽

Basem Kanawati ◽

Alesia Walker ◽

Bernhard Michalke

Keyword(s):

Oxidative Stress ◽

Rat Brain ◽

Brain Tissue ◽

Markers Of Oxidative Stress ◽

Rat Brain Tissue

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Liquid Chromatography Analysis of Clozapine in Rat Brain Tissue, Using its Molecularly Imprinted Polymer after Administration of Toxic Dose of Drug and Lipid Emulsion Therapy

Current Pharmaceutical Analysis ◽

10.2174/1573412914666180111160741 ◽

2019 ◽

Vol 15 (3) ◽

pp. 251-257

Author(s):

Bahareh Sadat Yousefsani ◽

Seyed Ahmad Mohajeri ◽

Mohammad Moshiri ◽

Hossein Hosseinzadeh

Keyword(s):

Rat Brain ◽

Brain Tissue ◽

Molecularly Imprinted Polymer ◽

Lipid Emulsion ◽

Limit Of Detection ◽

Imprinted Polymer ◽

Toxic Dose ◽

Molecularly Imprinted ◽

The Brain ◽

Rat Brain Tissue

Background:Molecularly imprinted polymers (MIPs) are synthetic polymers that have a selective site for a given analyte, or a group of structurally related compounds, that make them ideal polymers to be used in separation processes.Objective:An optimized molecularly imprinted polymer was selected and applied for selective extraction and analysis of clozapine in rat brain tissue.Methods:A molecularly imprinted solid-phase extraction (MISPE) method was developed for preconcentration and cleanup of clozapine in rat brain samples before HPLC-UV analysis. The extraction and analytical process was calibrated in the range of 0.025-100 ppm. Clozapine recovery in this MISPE process was calculated between 99.40 and 102.96%. The limit of detection (LOD) and the limit of quantification (LOQ) of the assay were 0.003 and 0.025 ppm, respectively. Intra-day precision values for clozapine concentrations of 0.125 and 0.025 ppm were 5.30 and 3.55%, whereas inter-day precision values of these concentrations were 9.23 and 6.15%, respectively. In this study, the effect of lipid emulsion infusion in reducing the brain concentration of drug was also evaluated.Results:The data indicated that calibrated method was successfully applied for the analysis of clozapine in the real rat brain samples after administration of a toxic dose to animal. Finally, the efficacy of lipid emulsion therapy in reducing the brain tissue concentration of clozapine after toxic administration of drug was determined.Conclusion:The proposed MISPE method could be applied in the extraction and preconcentration before HPLC-UV analysis of clozapine in rat brain tissue.

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The Biosynthesis of a Disialylganglioside by Galactosyltransferase from Rat Brain Tissue

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)45432-x ◽

1972 ◽

Vol 247 (8) ◽

pp. 2322-2327

Author(s):

Frederico A. Cumar ◽

John F. Tallman ◽

Roscoe O. Brady

Keyword(s):

Rat Brain ◽

Brain Tissue ◽

Rat Brain Tissue

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High-fat diet-induced obesity and impairment of brain neurotransmitter pool

Translational Neuroscience ◽

10.1515/tnsci-2020-0099 ◽

2020 ◽

Vol 11 (1) ◽

pp. 147-160

Author(s):

Ranyah Shaker M. Labban ◽

Hanan Alfawaz ◽

Ahmed T. Almnaizel ◽

Wail M. Hassan ◽

Ramesa Shafi Bhat ◽

...

Keyword(s):

Oxidative Stress ◽

Brain Tissue ◽

High Fat Diet ◽

Density Lipoprotein ◽

Obese Group ◽

Control Group ◽

High Fat ◽

Brain Neurotransmitter ◽

The Brain ◽

Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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