scholarly journals Discovering the Protective Effects of Resveratrol on Aflatoxin B1-Induced Toxicity: A Whole Transcriptomic Study in a Bovine Hepatocyte Cell Line

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1225
Author(s):  
Marianna Pauletto ◽  
Mery Giantin ◽  
Roberta Tolosi ◽  
Irene Bassan ◽  
Andrea Barbarossa ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Line ◽  
Aflatoxin B1 ◽  
Molecular Mechanisms ◽  
Natural Antioxidants ◽  
Protective Role ◽  
Economic Losses ◽  
Protective Effects ◽  
Hepatocyte Cell Line ◽  
Group I

Aflatoxin B1 (AFB1) is a natural feed and food contaminant classified as a group I carcinogen for humans. In the dairy industry, AFB1 and its derivative, AFM1, are of concern for the related economic losses and their possible presence in milk and dairy food products. Among its toxic effects, AFB1 can cause oxidative stress. Thus, dietary supplementation with natural antioxidants has been considered among the strategies to mitigate AFB1 presence and its toxicity. Here, the protective role of resveratrol (R) has been investigated in a foetal bovine hepatocyte cell line (BFH12) exposed to AFB1, by measuring cytotoxicity, transcriptional changes (RNA sequencing), and targeted post-transcriptional modifications (lipid peroxidation, NQO1 and CYP3A enzymatic activity). Resveratrol reversed the AFB1-dependent cytotoxicity. As for gene expression, when administered alone, R induced neglectable changes in BFH12 cells. Conversely, when comparing AFB1-exposed cells with those co-incubated with R+AFB1, greater transcriptional variations were observed (i.e., 840 DEGs). Functional analyses revealed that several significant genes were involved in lipid biosynthesis, response to external stimulus, drug metabolism, and inflammatory response. As for NQO1 and CYP3A activities and lipid peroxidation, R significantly reverted variations induced by AFB1, mostly corroborating and/or completing transcriptional data. Outcomes of the present study provide new knowledge about key molecular mechanisms involved in R antioxidant-mediated protection against AFB1 toxicity.

scholarly journals Triptolide Attenuates Vascular Calcification by Upregulating Expression of miRNA-204

2021 ◽  
Vol 11 ◽  
Author(s):  
Yu-qiang Pei ◽  
Yong-qiu Zheng ◽  
Yao-dong Ding ◽  
Qi-xiang Xu ◽  
Di Cao ◽  
...  
Keyword(s):  
Vascular Calcification ◽  
Molecular Mechanisms ◽  
Therapeutic Option ◽  
Calcium Content ◽  
Rat Aorta ◽  
Protective Role ◽  
Bone Morphogenetic Protein 2 ◽  
Dependent Manner ◽  
Protective Effects ◽  
Alp Activity

Background: Triptolide (TP), a naturally derived compound from Tripterygium wilfordii, has been proven effective in protecting against cardiovascular system, but the molecular mechanisms underlying its protective effects are poorly understood. In the current study, we sought to test the potential protective role of TP in the regulation of vascular calcification in a rat model and explore whether TP attenuates medial vascular calcification by upregulating miRNA-204.Methods: Vitamin D3 plus nicotine (VDN) was used to induce a vascular calcification (VC) model of rat aorta. Von Kossa and Hematoxylin-Eosin staining were applied to assess the degree of calcification of rat aortas. Calcium content and alkaline phosphatase activity were measured. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was applied to quantify miRNA-204 expression. The localization of runt-related transcription factor-2 (RUNX2) and bone morphogenetic protein-2 (BMP2) expressions were detected by immunohistochemistry and western blotting.Results: Administration of TP greatly reduced vascular calcification in a dose-dependent manner compared with VC controls. The increase in ALP activity and calcium content was ameliorated by TP. Moreover, protein expression levels of BMP2 and RUNX2 were significantly reduced in calcified aortas. MiRNA-204 expression was increased in the TP-treated groups compared with VC controls and the effects of TP were reversed by the intravenous injection of miRNA-204-interfering lentivirus. However, the miRNA-204-overexpressing lentivirus had no additional effects on ALP activity, calcium content, BMP2 and RUNX2 expressions compared with those from TP group.Conclusion: TP inhibited BMP2 and RUNX2 expression and attenuated vascular calcification via upregulating the level of miRNA-204. TP appears to be a potential new therapeutic option for treating vascular calcification.

scholarly journals Investigation of the Protective Effects of Taurine against Alloxan-Induced Diabetic Retinal Changes via Electroretinogram and Retinal Histology with New Zealand White Rabbits

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Samuel Tung-Hsing Chiang ◽  
Shang-Min Yeh ◽  
Yi-Chen Chen ◽  
Shiun-Long Lin ◽  
Jung-Kai Tseng
Keyword(s):  
Body Weight ◽  
Protective Role ◽  
The Body ◽  
Antidiabetic Activity ◽  
Protective Effects ◽  
Group Iii ◽  
Glucose Levels ◽  
Diabetic Retina ◽  
Group I ◽  
Group Ii

The purpose of this study was to investigate the protective role of orally administered taurine against diabetic retinal changes via electroretinogram (ERG) and retinal histology on rabbits. Rabbits were randomly assigned into groups: Group I (vehicle administration only); Group II (diabetes: induced by 100 mg/kg alloxan injection); Group III (diabetes and fed with 200 mg/kg taurine); and Group IV (diabetes and fed with 400 mg/kg taurine). The body weight and blood glucose levels of the rabbits were monitored weekly. The ERG was measured on weeks 5 and 15. Retinal histology was analyzed in the end of the experiment. Results revealed that a taurine supplement significantly ameliorates the alloxan-induced hyperglycemia and protects the retina from electrophysiological changes. Group II showed a significant(P<0.05)change in the mean scotopic b-wave amplitude when compared to that of Group I, whereas the diabetic rabbits treated with taurine (Group III and IV) were analogous to Group I. Histologically, the amount of Bipolar and Müller cells showed no difference(P>0.05)between all groups and when compared with those of Group I. Our study provides solid evidences that taurine possesses an antidiabetic activity, reduced loss of body weight, and less electrophysiological changes of the diabetic retina.

scholarly journals Acrylamide Induced Oxidative Cellular Senescence in Embryonic Fibroblast Cell Line (NIH 3T3): A Protection by Carvacrol

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Mehdi Evazalipour ◽  
Pouya Safarzadeh Kozani ◽  
Pooria Safarzadeh Kozani ◽  
Sahar Shabani ◽  
Bahar Rezaei Soufi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cell Line ◽  
Cellular Senescence ◽  
Fibroblast Cell ◽  
Protective Effects ◽  
Proliferating Cells ◽  
Beneficial Effects ◽  
Nih 3T3 ◽  
Embryonic Fibroblast

Background: Stress-induced cellular senescence is a perpetual state of cell cycle arrest occurring in proliferating cells in response to stressful conditions. It is believed that oxidative stress plays a unique role in this process. As a reactive chemical compound that can induce oxidative stress, acrylamide is widely applied in several fields. Carvacrol is a liquid phenolic monoterpenoid found in essential oils of some plants and is known for its antioxidant and anticarcinogenic properties. Objectives: The current study aimed to evaluate the effects of carvacrol on oxidative stress and cellular senescence induced by acrylamide in the NIH 3T3 cell line. Methods: NIH 3T3 embryonic fibroblast cells were exposed to different concentrations of acrylamide, carvacrol, and H2O2 in a cell culture medium. The level of β-galactosidase (SA-β-gal) activity, as a marker of cellular senescence, was measured using staining and quantitative assays. Furthermore, to measure oxidative stress parameters, the content of glutathione and lipid peroxidation were determined. Results: Acrylamide could induce premature senescence evident by the elevated lipid peroxidation and SA-β-gal activity and declined cell viability and glutathione. Moreover, carvacrol showed beneficial effects on both acrylamide- and H2O2-induced cellular senescence by significantly reversing or subsiding the effect of oxidative stress and mediating its consequences. Conclusions: It can be concluded that carvacrol has protective effects against oxidative cellular senescence induced by acrylamide in the NIH 3T3 cell line.

Haematological and biochemical toxicity induced by methanol in rats: Ameliorative effects of Opuntia vulgaris fruit extract

2011 ◽  
Vol 30 (12) ◽  
pp. 1963-1971 ◽  
Author(s):  
Mongi Saoudi ◽  
Samira Jebahi ◽  
Kamel Jamoussi ◽  
Ghada Ben Salah ◽  
Choumous Kallel ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Total Protein ◽  
Natural Antioxidants ◽  
Treated Group ◽  
Protective Effects ◽  
Fruit Extract ◽  
Serum Total Protein ◽  
Potential Source ◽  
Antioxidant Enzymes Activities

The ameliorative effects of Opuntia vulgaris fruit extract (OE) were evaluated against methanol-induced haematological and biochemical toxicity in rats. The methanol-induced haematological and biochemical perturbation significantly decreased the levels of red blood cell (RBC), haemoglobin (Hb), haematocrit (Ht), serum total protein and increased glucose, cholesterol, and triglyceride levels in serum. Treatment of rats with methanol significantly increased lipid peroxidation (LPO) level and decreased the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in erythrocytes. OE treatment could increase significantly the levels of RBC, Hb, Ht and total protein, and decrease glucose, cholesterol and triglyceride levels in serum, and increase the activities of SOD, CAT and GPx in erythrocytes, when compared with methanol-treated group. Spleen histopathology showed that OE could significantly reduce the incidence of spleen lesion induced by methanol. These results suggested that OE could exhibit a potential source of natural antioxidants against methanol-induced haematological and biochemical disruption in rats. The protective effects of OE may be due to the modulation of antioxidant enzymes activities and inhibition of LPO.

Enhancement of survival by LPA via Erk1/Erk2 and PI 3-kinase/Akt pathways in a murine hepatocyte cell line

2001 ◽  
Vol 281 (6) ◽  
pp. C2010-C2019 ◽  
Author(s):  
Yuri Y. Sautin ◽  
James M. Crawford ◽  
Stanislav I. Svetlov
Keyword(s):  
Cell Line ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Protective Effects ◽  
Hepatocellular Injury ◽  
Cell Protection ◽  
Lpa Receptor ◽  
Hepatocyte Cell Line ◽  
Tnf Α ◽  
Murine Hepatocyte

First published September 5, 2001; 10.1152/ajpcell.00077.2001.—Protective mechanisms for lysophosphatidic acid (LPA) against cell death caused by Clostridium difficile toxin, or tumor necrosis factor-α (TNF-α) plus d-galactosamine, were investigated in a murine hepatocyte cell line AML12 expressing Edg2 LPA receptor. In these models of hepatocellular injury, LPA prevented hepatocyte damage, suppressed apoptosis, and enhanced cell survival in a dose-dependent fashion. The protective effects of LPA were abolished by wortmannin and LY-294002, specific inhibitors of phosphatidylinositol 3-phosphate kinase (PI 3-kinase), and by PD-98059 and U-0126, inhibitors of MEK1/MEK2. In nontreated hepatocytes, LPA elicited a gradual and sustained increase in phosphorylation of Erk1/Erk2 over 180 min of stimulation and downstream phosphorylation of p90RSK and transcription factor Elk-1. In C. difficile toxin-treated cells, LPA-induced phosphorylation of Erk1/Erk2 was rapid but transient, while p90RSK and Elk-1 phosphorylation did not change significantly. LPA stimulated phosphorylation of Akt in a time-dependent manner in both intact and toxin-treated AML12 hepatocytes. Wortmannin and LY-294002 abolished phosphorylation of Akt, further supporting activation of PI 3-kinase/Akt as a signaling pathway, which mediates hepatocyte protection by LPA. Taken together, these results demonstrate that LPA prevents cell apoptosis induced by C. difficile toxin and TNF-α/d-galactosamine in the AML12 murine hepatocyte cell line. Cell protection by LPA involves activation of the mitogen-activated protein kinase Erk1/Erk2 cascade and PI 3-kinase-dependent phosphorylation of Akt.

scholarly journals Aflatoxin B1 Toxicity in Zebrafish Larva (Danio rerio): Protective Role of Hericium erinaceus

Toxins ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 710
Author(s):  
Davide Di Paola ◽  
Carmelo Iaria ◽  
Fabiano Capparucci ◽  
Marika Cordaro ◽  
Rosalia Crupi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Aflatoxin B1 ◽  
Protective Role ◽  
Fish Feed ◽  
Fish Development ◽  
Hericium Erinaceus ◽  
Morphological Alterations ◽  
Oxidative Stress Pathway ◽  
Antioxidant Defense Systems

Aflatoxin B1 (AFB1), a secondary metabolite produced by fungi of the genus Aspergillus, has been found among various foods as well as in fish feed. However, the effects of AFB1 on fish development and its associated toxic mechanism are still unclear. In the present study, we confirmed the morphological alterations in zebrafish embryos and larvae after exposure to different AFB1 doses as well as the oxidative stress pathway that is involved. Furthermore, we evaluated the potentially protective effect of Hericium erinaceus extract, one of the most characterized fungal extracts, with a focus on the nervous system. Treating the embryos 6 h post fertilization (hpf) with AFB1 at 50 and 100 ng/mL significantly increased oxidative stress and induced malformations in six-day post-fertilization (dpf) zebrafish larvae. The evaluation of lethal and developmental endpoints such as hatching, edema, malformations, abnormal heart rate, and survival rate were evaluated after 96 h of exposure. Hericium inhibited the morphological alterations of the larvae as well as the increase in oxidative stress and lipid peroxidation. In conclusion: our study suggests that a natural extract such as Hericium may play a partial role in promoting antioxidant defense systems and may contrast lipid peroxidation in fish development by counteracting the AFB1 toxicity mechanism.

Synergistic protective role of mirazid (Commiphora molmol) and ascorbic acid against tilmicosin-induced cardiotoxicity in mice

2015 ◽  
Vol 93 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Mohamed M. Abdel-Daim ◽  
Emad W. Ghazy ◽  
Mostafa Fayez
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Antioxidant Activities ◽  
Cardiac Injury ◽  
Elevated Serum ◽  
Radical Scavenging ◽  
Serum Levels ◽  
Protective Role ◽  
Protective Effects ◽  
Cardiac Damage

Tilmicosin (TIL) is a long-acting macrolide antibiotic approved for the treatment of cattle with Bovine Respiratory Disease. However, overdose of TIL has been reported to induce cardiotoxicity. The purpose of our experiment was to evaluate the protective effects of Commiphora molmol (mirazid (MRZ); myrrh) and (or) ascorbic acid (AA) against TIL-induced cardiotoxicity in mice. MRZ and AA were orally administered using stomach gavage, either alone or in combination for 5 consecutive days, followed with a single TIL overdose. TIL overdose induced a significant increase in serum levels of cardiac damage biomarkers (AST, LDH, CK, CK-MB, and cTnT), as well as cardiac lipid peroxidation, but cardiac levels of antioxidant biomarkers (GSH, SOD, CAT, and TAC) were decreased. Both MRZ and AA tended to normalize the elevated serum levels of cardiac injury biomarkers. Furthermore, MRZ and AA reduced TIL-induced lipid peroxidation and oxidative stress parameters. MRZ and AA combined produced a synergistic cardioprotective effect. We conclude that myrrh and (or) vitamin C administration minimizes the toxic effects of TIL through their free-radical-scavenging and potent antioxidant activities.

scholarly journals Punicalagin Exerts Protective Effects against Ankylosing Spondylitis by Regulating NF-κB-TH17/JAK2/STAT3 Signaling and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Xinzhe Feng ◽  
Qinyuan Yang ◽  
Chen Wang ◽  
Wenwen Tong ◽  
Weidong Xu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ankylosing Spondylitis ◽  
Inflammatory Mediators ◽  
Antioxidant Status ◽  
Serum Levels ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Protective Effects ◽  
Stat3 Signaling

Background. Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by sacroiliitis and spinal rigidity of the axial joints. The role of oxidative stress and increased proinflammatory cytokines is well documented in AS pathogenesis. Punicalagin (2,3-hexahydroxydiphenoyl-gallagyl-D-glucose), an ellagitannin widely present in pomegranates, is found to exhibit potent anti-inflammatory, antiproliferative, and antioxidative effects. The present study was undertaken to investigate the effects of punicalagin in a rodent model of AS. Methods. BALB/c mice induced spondylitis were sacrificed 24 h after the last injection of proteoglycan extract. Histological scoring was done to assess the degree of the disease. The expression of JAK2/STAT3 proteins and proteins of the nuclear factor-κB (NF-κB) pathway was determined by immunoblotting. Serum levels of inflammatory mediators—TNF-α, IL-1β, IL-6, IL-17A, and IL-23—were assessed. Levels of lipid peroxidation and reactive oxygen species (ROS) were quantified. Antioxidant status as a measure of activities of antioxidant enzymes—catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)—was determined. Results. Punicalagin effectively improved antioxidant status and decreased lipid peroxidation, ROS production, and serum levels of inflammatory mediators. NF-κB pathway and JAK2/STAT3 signaling were significantly (p<0.05) downregulated. Punicalagin effectively regulated the production of cytokines by the Th17 cells and the IL-17A/IL-23 axis. Conclusion. The observations suggest that punicalagin exerts a protective role in AS via reducing oxidative stress and regulating NF-κB/TH17/JAK2/STAT3 signal. Punicalagin thus could be explored further as a potent candidate compound in the treatment of AS.

scholarly journals Evaluation of Neuroprotective Effects of Quercetin against Aflatoxin B1-Intoxicated Mice

Animals ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 898 ◽  
Author(s):  
Enrico Gugliandolo ◽  
Alessio Filippo Peritore ◽  
Ramona D’Amico ◽  
Patrizia Licata ◽  
Rosalia Crupi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Aflatoxin B1 ◽  
Protective Effects ◽  
Behavioral Alterations ◽  
Sod Activity ◽  
Neuroprotective Effects ◽  
Oxidative Stress Pathway ◽  
Ameliorative Effect ◽  
The Brain

Aflatoxin B1 (AFB1) is a mycotoxin commonly present in feed, characterized by several toxic effects. AFB1 seems to have a neurotoxical effect that leads to memory impairment behavior. AFB1 toxicity involves the induction of the oxidative stress pathway, rising lipid peroxidation, and it decreases antioxidant enzyme levels. Hence, in our research, we wanted to evaluate the potential protective effects of quercetin 30 mg/kg in AFB1-mediated toxicity in the brain and the ameliorative effect on behavioral alterations. Oral supplementation with quercetin increased glutathione peroxidase (GSH) levels, superoxidedismutase (SOD) activity and catalase (CAT) in the brain, and it reduced lipid peroxidation in AFB1-treated mice. This antioxidant effect of quercetin in the brains of AFB1-intoxicated mice is reflected in better cognitive and spatial memory capacity, as well as a better profile of anxiety and lethargy disorders. In conclusion, our study suggests that quercetin exerts a preventive role against oxidative stress by promoting antioxidative defense systems and limiting lipid peroxidation.

Effect of pycnogenol and spirulina on vancomycin-induced renal cortical oxidative stress, apoptosis, and autophagy in adult male albino rat

2016 ◽  
Vol 94 (8) ◽  
pp. 838-848 ◽  
Author(s):  
Naglaa A. Bayomy ◽  
Eman Z. Abdelaziz ◽  
Mona A. Said ◽  
Marwa S. Badawi ◽  
Reda H. El-Bakary
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Elevated Serum ◽  
Natural Antioxidants ◽  
Control Group ◽  
Protective Effects ◽  
Drug Induced ◽  
Albino Rat ◽  
Group I ◽  
Vancomycin Group

Vancomycin-induced nephrotoxicity has been reported to occur in 5%–25% of patients who were administered with it. Several natural antioxidants were found to be effective against drug-induced toxicity. We evaluated the possible protective effects of spirulina and pycnogenol alone or in combination on vancomycin-induced renal cortical oxidative stress. Forty-nine rats were randomly divided into 7 groups: group I, control; group II, received spirulina 1000 mg/kg per day; group III, received pycnogenol 200 mg/kg per day; group IV, received vancomycin 200 mg/kg per day every 12 h; group V, (spirulina + vancomycin); group VI, (pycnogenol + vancomycin); and group VII, (pycnogenol + spirulina + vancomycin). At the end of the experiment, kidney functions were estimated and then the kidneys were removed, weighed, and sampled for histopathological, immunohistochemistry, and biochemical studies. Administration of spirulina and pycnogenol alone or in combination decreased elevated serum creatinine, blood urea nitrogen, renal malondialdehyde, and immunoexpression of the proapoptotic protein (Bax), autophagic marker protein (LC3/B), and inducible nitric oxide synthase induced by vancomycin. They increased reduced glutathione, glutathione peroxidase, superoxide dismutase, and immunoexpression of the antiapoptotic protein (Bcl2). They also ameliorated the morphological changes induced by vancomycin. The combination therapy of spirulina and pycnogenol showed better protective effects than the corresponding monotherapy.

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