Resveratrol Relieved Acute Liver Damage in Ducks (Anas platyrhynchos) Induced by AFB1 via Modulation of Apoptosis and Nrf2 Signaling Pathways

The presence of aflatoxin B1 (AFB1) in feed is a serious threat to livestock and poultry health and to human food safety. Resveratrol (Res) is a polyphenolic compound with antioxidant, anti-apoptotic and other biological activities; however, it is not clear whether it can improve AFB1 induced hepatotoxicity. Therefore, this study was conducted to investigate the effects of dietary Res on liver injury induced by AFB1 and its mechanisms. A total of 270 one-day-old male specific pathogen free (SPF) ducks, with no significant difference in weight, were randomly assigned to three groups: the control group, the AFB1 group and the AFB1 + Res group, which were fed a basic diet, a basic diet and a basic diet containing 500 mg/kg Res, respectively. On the 70th day, the ducks in theAFB1 group and the AFB1+ 500 mg/kg Res group were given 60 μg/kg AFB1 via gavage. When comparing the AFB1 group and the AFB1 + Res group and also with the control group, AFB1 significantly increased liver damage, cytochrome P450 (CYP450) and AFB1-DNA adduct content, increased oxidative stress levels and induced liver apoptosis, which was improved by Res supplementation. In sum, the addition of Res to feed can increase the activity of the II-phase enzyme, activate the nuclear factor E2-related factor 2 (Nrf2) signal pathway, and protect ducks’ livers from the toxicity, oxidative stress and inflammatory reaction induced by AFB1.

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Vinpocetine attenuates fluoxetine-induced liver damage in rats; Role of Nrf2 and PPAR-γ

Human & Experimental Toxicology ◽

10.1177/09603271211051597 ◽

2021 ◽

pp. 096032712110515

Author(s):

Gellan Alaa Mohamed Kamel

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Mrna Expression ◽

Liver Damage ◽

B Cell Lymphoma ◽

Control Group ◽

Related Factor ◽

Protective Effects ◽

Ppar Γ

Background Fluoxetine (FLX) has been widely used as first-line treatment in cases of depression and other neuropsychiatric disorders. Although its safety has been approved, the use of FLX was associated with liver injury and chronic liver disease. Vinpocetine (Vinpo), a nootropic drug, possesses antioxidant and anti-inflammatory effects. Objective This study aimed to evaluate the protective effects of Vinpo on FLX-induced liver damage pointing to the role of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and nuclear factor erythroid 2-related factor 2 (Nrf2). Methods Rats were randomized to four groups: control group, Vinpo group (20 mg/kg/day; orally), FLX group (10 mg/kg/day; orally), and Vinpo + FLX group. Results FLX-induced liver damage was evidenced through elevated liver function biomarkers and induced hepatic histopathological changes. Concurrent Vinpo treatment resulted in a significant decrease in hepatotoxicity biomarkers and histopathological alterations. FLX-induced oxidative stress and inflammation were attenuated by Vinpo. In addition, Vinpo attenuated the hepatic NRF2 and HO-1 levels and up-regulated PPAR-γ expression. Moreover, FLX elevated Bcl-2-associated X protein (Bax) mRNA expression and decreased B-cell lymphoma 2 (Bcl2) mRNA expression were markedly reversed by Vinpo. Conclusion Vinpo possesses ameliorative effects against FLX-induced liver injury in rats. This effect may be due to attenuation of oxidative stress and inflammation, in addition to upregulation of PPAR-γ expression.

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Association Between Magnesium and Oxidative Stress in Patients with Obesity

Current Nutrition & Food Science ◽

10.2174/1573401315666190730123842 ◽

2020 ◽

Vol 16 (5) ◽

pp. 743-748

Author(s):

Ana R.S. de Oliveira ◽

Kyria J.C. Cruz ◽

Jennifer B.S. Morais ◽

Juliana S. Severo ◽

Jéssica B. Beserra ◽

...

Keyword(s):

Oxidative Stress ◽

Thiobarbituric Acid ◽

Magnesium Concentration ◽

Control Group ◽

Compensatory Mechanism ◽

Thiobarbituric Acid Reactive Substances ◽

Magnesium Intake ◽

Significant Difference ◽

Dietary Magnesium ◽

And Control

Background: The role of minerals in preventing the generation of oxidative stress in obese individuals has been evaluated. Magnesium is an antioxidant nutrient and a cofactor of enzymes involved in the cell membrane stabilization, attenuating the effects of oxidative stress. Objective: To evaluate the association between magnesium and concentrations of thiobarbituric acid reactive substances (TBARS) in patients with obesity and eutrophic women. Methods: A cross-sectional study was conducted with 73 women, divided into two groups: case group (patients with obesity, n=27) and control group (eutrophic women, n=46). Measurements of body mass index and waist circumference were performed. Dietary magnesium intake was assessed by the three-day food record using the NutWin software. Urinary magnesium concentration was measured by atomic absorption spectrophotometry method. Plasma concentrations of thiobarbituric acid reactive substances (TBARS) were also determined. Results: Mean values of dietary magnesium intake were 161.59 ± 60.04 and 158.73 ± 31.96 for patients with obesity and control group, respectively, with no significant difference between the groups studied (p >0.05). The value of urinary excretion of magnesium was lower than the reference values in both groups, with no significant difference between the groups studied (p >0.05). The plasma concentration of thiobarbituric acid reactive substances was significantly higher in patients with obesity compared to the control group (p <0.001). There was no correlation between levels of magnesium biomarkers and the concentration of TBARS (p >0.05). Conclusion: Patients with obesity showed a reduced dietary magnesium intake which seems to induce hypomagnesuria as a compensatory mechanism. The marker of oxidative stress evaluated in this study was not influenced by magnesium.

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

Molecules ◽

10.3390/molecules26051332 ◽

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.

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Protective effect of GSK-3β/Nrf2 mediated by dimethyl fumarate in middle cerebral artery embolization reperfusion rat model

Current Neurovascular Research ◽

10.2174/1567202618666211109105024 ◽

2021 ◽

Vol 18 ◽

Author(s):

Yuan Li ◽

Lan Chu ◽

Chunfeng Liu ◽

Zongyi Zha ◽

Yuanlu Shu

Keyword(s):

Oxidative Stress ◽

Protective Effect ◽

Sham Group ◽

Infarct Volume ◽

Dimethyl Fumarate ◽

Control Group ◽

Related Factor ◽

Nissl Staining ◽

Gsk 3Β ◽

Nrf2 Expression

Aim: This study investigated the protective effect of dimethyl fumarate (DMF) in rats by mediating GSK3-β/Nrf2 using the middle cerebral artery embolization reperfusion (MCAO/R) rat model. Background: After an acute ischemic stroke (AIS), oxidative stress occurs. Dimethyl fumarate (DMF), a nuclear factor-E2-related factor 2 (Nrf2) activator, approved by the US Food and Drug Administration (FDA), was observed to regulate the Nrf2 pathway by acting as an anti-oxidative stress agent; however, whether this agent is involved in inhibiting GSK-3β remains to be established. Methods: DMF model was used to explore the effects of GSK-3β on Nrf2 expression level, Nrf2-ARE binding activity and Nrf2/ARE downstream expression level of anti-oxidant stress protein in Cerebral ischemia-reperfusion injury (CIRI). 60 rats were randomly divided into Sham group, MCAO/R group, solvent control group (DMSO group) and DMF treatment group, with 15 rats in each group. The MCAO/R, DMSO and DMF groups were considered in the MCAO/R model using the modified thread embolization method. In contrast, the Sham group was only anaesthetized and disinfected, and tissue muscle was dissected without inserting suture emboli. DMF group was gavaged with 45mg/kg per day of DMF, DMSO control group was gavaged with DMSO of equal volume, while MCAO/R group was only modeled without any intragastric treatment. The rats were treated seven days after the operation, and a neurological function Longa score was estimated. The rats were sacrificed seven days later, and the infarct volume was assessed by TTC staining. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in rat brain tissue. Nissl staining was used to observe the expression of neurons in the infarcted cortex. Western blotting (WB) was used to observe the protein expression levels of glycogen synthase kinase 3β(GSK-3β), nuclear factor E2-related factor 2 (Nrf2), downstream heme oxygenase 1 (HO1) and NADPH quinone oxidoreductase 1 (NQO1) in four groups. The expression levels of GSK-3β and Nrf2 in the four groups were observed by immunohistochemistry and immunofluorescence. Results: (1) The Longa score of the MCAO/R, DMSO and DMF groups was found to be higher compared to the Sham group, indicating successful operation. The Longa score of the DMF group was lower than that of the other three groups 4-7 days after surgery (P<0.05). (2) HE and Nissl staining showed that the DMF group had lower neuron necrosis and higher gliosis compared to the control groups. (3) TTC staining results showed that the infarct volume of the DMF group was significantly smaller than the MCAO/R and DMSO groups. (4) Protein results showed that the GSK-3β expression in the DMF group was lower than that in all groups, while the expression of Nrf2, HO1 and NQO1 was higher compared to other groups. Conclusion: DMF can reduce neurological deficits and infarct size in the MCAO/R model. The protective effect may be related to decreased GSK-3β expression and increased Nrf2 expression, which may play a role in anti-oxidative stress.

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Changes in oxidation-antioxidation function on the thymus of chickens infected with reticuloendotheliosis virus

BMC Veterinary Research ◽

10.1186/s12917-020-02708-6 ◽

2020 ◽

Vol 16 (1) ◽

Author(s):

Dahan Yang ◽

Chenhui Zhao ◽

Meixi Zhang ◽

Shujun Zhang ◽

Jie Zhai ◽

...

Keyword(s):

Oxidative Stress ◽

Control Group ◽

Reticuloendotheliosis Virus ◽

Antioxidative Function ◽

Group I ◽

Antioxidant Function ◽

Thymus Atrophy ◽

The Status ◽

Specific Pathogen

Abstract Background Reticuloendotheliosis virus (REV) is a retrovirus that causes severe immunosuppression in poultry. Animals grow slowly under conditions of oxidative stress. In addition, long-term oxidative stress can impair immune function, as well as accelerate aging and death. This study aimed to elucidate the pathogenesis of REV from the perspective of changes in oxidative-antioxidative function following REV infection. Methods A total of 80 one-day-old specific pathogen free (SPF) chickens were randomly divided into a control group (Group C) and an REV-infected group (Group I). The chickens in Group I received intraperitoneal injections of REV with 104.62/0.1 mL TCID50. Thymus was collected on day 1, 3, 7, 14, 21, 28, 35, and 49 for histopathology and assessed the status of oxidative stress. Results In chickens infected with REV, the levels of H2O2 and MDA in the thymus increased, the levels of TAC, SOD, CAT, and GPx1 decreased, and there was a reduction in CAT and Gpx1 mRNA expression compared with the control group. The thymus index was also significantly reduced. Morphological analysis showed that REV infection caused an increase in the thymic reticular endothelial cells, inflammatory cell infiltration, mitochondrial swelling, and nuclear damage. Conclusions These results indicate that an increase in oxidative stress enhanced lipid peroxidation, markedly decreased antioxidant function, caused thymus atrophy, and immunosuppression in REV-infected chickens.

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The The Role Of Von Willenbrand Factors As The Early Detection Of Endotel Cell Damage In Youth Ages With Obesity In The Usu Medan Campus Environment

ABDIMAS TALENTA: Jurnal Pengabdian Kepada Masyarakat ◽

10.32734/abdimastalenta.v6i1.5865 ◽

2021 ◽

Vol 6 (1) ◽

pp. 179-181

Author(s):

Rusdiana ◽

Muhammad Syahputra ◽

Sry Suryani

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Vascular System ◽

Cell Damage ◽

Single Layer ◽

Control Group ◽

Research Subjects ◽

Cross Sectional ◽

Significant Difference ◽

Obese Subjects

Preliminary : Endothelial cells are a single layer that lines the entire vascular system. Endothelial dysfunction can be triggered by several main things, namely physical stress, oxidative stress and irritant substances. Obesity triggers an inflammatory process and metabolic disorders that will lead to increased oxidative stress. Long-term oxidative stress will cause damage to cells and tissues and trigger degenerative diseases. Damage to endothelial cells is expected to be detected by examining Von Willenbrand levels so that it can prevent complications of vascular disorders early. Method: This research is descriptive with cross sectional design. Carried out from March to October 2018 on the USU Campus. The first examination was done to measure body weight and height to determine body mass index, then performed lipid profile and blood sugar levels (KGD) in the sample, then examined von Willenbrand factor levels carried out in the integrated laboratory of USU FK using the method ELISA in both the sample group and the control group. The research subjects were adolescents aged 17-25 years with BMI> 25 kg / m2Data analysis was carried out using the T-Test statistical program, comparing two groups. Result: Of the 40 obese subjects found Von Wilenbrand level values The lowest factor was 1.78 IU / ml and the highest was 35.60 IU / ml. Whereas in 40 non-obese subjects Von Wilenbrand grade values were the lowest factor of 2.01 IU / ml and the highest was 45.10 IU / ml. This difference was not statistically significant (p = 0.661).Conclusion: There was no significant difference between the levels of Von Wilenbrand Factors in obese subjects with non-obese subjectsKey Words: Obesity, endothelial cells, Von Wilenbrand Factors

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Perbedaan Kadar Glutation (GSH) Hepar Tikus Putih Jantan (Rattus norvegicus) yang diinduksi Parasetamol Dosis Toksik dengan Pemberian Ekstrak Daun Kelor (Moringa oleifera)

Jurnal Ilmiah Universitas Batanghari Jambi ◽

10.33087/jiubj.v20i1.881 ◽

2020 ◽

Vol 20 (1) ◽

pp. 247

Author(s):

Nur Insani ◽

H.M.T Kamaluddin ◽

Swanny Swanny

Keyword(s):

Oxidative Stress ◽

Treatment Group ◽

Leaf Extract ◽

The Body ◽

Control Group ◽

Bb Rat ◽

Toxic Dose ◽

Experimental Animals ◽

Significant Difference ◽

Group Ii

Glutathione (GSH) transferase deficiency due to paracetamol exposure causes further oxidative stress to liver necrosis. To reduce oxidative stress that can cause damage to the liver of the body requires antioxidants. One plant to treat liver disease is the kelor leaf (because it has an active flavonoid material also has antioxidant activity). This study was conducted to determine the difference of glutathione hepar levels of male white rat induced paracetamol toxic dose by giving kelor leaf extract. The type of research is experimental laboratory in vivo with rancagan randomized post test only control group design. With the stages as follows 1.Leaf Extract Kelor with Ethanol 96%, 2.Perpeteration of experimental animals, 3.Treatment of experimental animals by giving extract of 3-dose of kelor leaf that is KP I 250 mg / 200 gr BB rat, KP II 500 mg / 200 gr BB rat, KP III 1000 mg / 200 gr BB rat for 14 days combined with paracetamol dose 2 gr / 200 gr BB rat compared with the negative control group (group given only paracetamol dose 2 gr / 200 gr BB rat) and control group positif only fed regular feed for 14 days). The result showed that there was a significant difference mean of GSH levels between all treatment groups obtained p = 0,000 (p <α) p values smaller than 0.05. There was the highest increase of GSH in treatment group II (142,7525 μmol / mg) and lowest dose of GSH in positive control group (57,1812 μmol / mg), dose paracetamol toxic dosage and kelor leaf extract 500 mg / gr BB rat can increase GSH hepar p = 0,000 (p <α) p less than 0 , 05. The conclusion of the test results showed that giving of kelor leaf extract at dose of treatment group II can increase GSH hepar level significantly

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The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

Caspian Journal of Neurological Sciences ◽

10.32598/cjns.7.24.5 ◽

2021 ◽

Vol 7 (1) ◽

pp. 42-50

Author(s):

Zahra Nazari Barchestani ◽

◽

Maryam Rafieirad ◽

Keyword(s):

Oxidative Stress ◽

Pain Threshold ◽

Male Rats ◽

Control Group ◽

Tail Flick ◽

Pain Thresholds ◽

Ischemic Group ◽

Significant Difference ◽

The Brain ◽

And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

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Propolis Protective Effects Against Doxorubicin-Induced Multi-Organ Toxicity via Suppression of Oxidative Stress, Inflammation, Apoptosis, and Histopathological Alterations in Female Albino Rats

Biointerface Research in Applied Chemistry ◽

10.33263/briac122.17621777 ◽

2021 ◽

Vol 12 (2) ◽

pp. 1762-1777

Keyword(s):

Oxidative Stress ◽

Large Scale ◽

Protective Efficacy ◽

Biological Activities ◽

Female Rats ◽

Control Group ◽

Albino Rats ◽

Protective Agent ◽

Protective Effects ◽

Treatment Protocols

Doxorubicin (DOX) is effective chemotherapy in several malignancies, but large-scale toxicities limit its clinical usefulness. Propolis has been reported to exhibit a broad spectrum of biological activities. We aim to assess the protective efficacy of propolis against DOX-induced multi-toxicity in female rats. Forty female rats were divided into four groups: control group; Group (P) were administrated oral propolis (100 mg/kg once daily for 28 days); Group (P+DOX) were injected with a single intraperitoneal dose of DOX (20 mg/kg i.p at 24th day after the propolis administration) and group (DOX) were injected with doxorubicin only. Estimation of cardiac, renal and hepatic injury markers, apoptosis and pro-inflammatory cytokines were done using sera. Also, liver and heart tissue samples were collected to determine GSH and MDA as oxidative stress markers. In addition to histopathological and immunohistochemical examination of Cytochrome-C and Connexin43 on lysed myocardium, liver, kidney and lung tissues. Doxorubicin toxicity caused marked deteriorations of measured parameters through the different mechanisms in different body organs. However, pre-treatment with propolis significantly ameliorated these alterations. Thus propolis can ameliorate the DOX-induced experimental multi-toxicity as cardiomyopathy, hepatotoxicity, nephritis and pneumonia. Thus, it could be a promising protective agent in DOX treatment protocols.

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CAT-21 A/T Gene Polymorphisms Associated with Breast Cancer Susceptibility

Bangladesh Journal of Medicine ◽

10.3329/bjm.v32i2.53792 ◽

2021 ◽

Vol 32 (2) ◽

pp. 79-84

Author(s):

Kevin Owen ◽

Siti Syarifah ◽

Mutiara Indah Sari

Keyword(s):

Breast Cancer ◽

Oxidative Stress ◽

Cancer Susceptibility ◽

Breast Cancer Susceptibility ◽

Healthy Control Group ◽

Control Group ◽

Genotype Distribution ◽

Significant Difference ◽

Pcr Rflp ◽

Healthy Control

Background: Oxidative stress induced cancer cell formation. Gene polymorphism plays roles in carcinogen metabolism, antioxidant and DNA repairing pathway was susceptibility to oxidative stress. This study aim to determine the association between CAT-21 A/T polymorphism with breast cancer susceptibility. Methods: Case control study was conducted on 65 breast cancer patient and 65 healthy control group. The whole blood samples were isolated from 65 breast cancer patients in Haji Adam Malik General Hospital Medan and 65 healthy control group. The CAT-21A/T polymorphism was analyzed by PCR-RFLP procedure. PCR-RFLP product was electrophoresed and visualized in agarose 4%. Results:The AA CAT-21 genotype were lower in breast cancer (BC) than healthy control (HC) group (31/47.7% vs 40/61.5%), in the contrary AT+TT genotype was greater in BC than HC group (34/52.3% vs 25/38.5%) with (p=0.159, OR=1.755, CI=0.874–3.525). A allele CAT-21 were found lower in BC than HC group (89/68.5% vs 105/80.8%) then T allele were greater in BC than HC group (41/31.5% vs 25/19.2%) with (p=0.033, OR=1.935;CI=1.022-3.428). Conclusions: There was significant difference in allele distribution of CAT-21 A/T between case and control group but no in genotype distribution. In this population study showed that allele of CAT -21 A/T polymorphism could represent as a risk factor to breast cancer. Bangladesh J Medicine July 2021; 32(2) : 79-84

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