Protective effects of bisoprolol against cadmium-induced myocardial toxicity through inhibition of oxidative stress and NF-κΒ signalling in rats

Abstract Introduction The aim of the study was to investigate the mitigative effects of bisoprolol (BIS) in cadmium-induced myocardial toxicity on oxidative stress and its inhibitive effect on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signalling in rats. Material and Methods Male albino Wistar rats were assigned to control, Cd, BIS 2 (2 mg/kg b.w.) and BIS 8 (8 mg/kg b.w.) groups with nine rats in each. Over four weeks, the control group was administered 1% gum acacia, all other groups received 3mg/kg b.w. CdCl2 dissolved in distilled water, and the BIS groups were additionally given bisoprolol in gum acacia. Blood samples were collected for biochemical estimations. Blood pressure and serum biomarker (lactate dehydrogenase, aspirate transaminase, alanine transferase and creatine kinase-MB, enzyme (superoxide dismutase, lipid hydroxy peroxidase, catalase and malondialdehyde), and tumour necrosis factor alpha (TNF-α) concentrations were measured. Western blot analysis was conducted for NF-κB and glutathione S-transferase (GST). After sacrificing the rats, cardiac tissue samples were examined histopathologically. Results Our findings pointed to a significant decrease (P < 0.05) in the studied serum biomarkers and levels of the relevant enzymes in the BIS 8 group compared to the Cd group. A significant decrease (P < 0.05) in NF-kB p65 expression and TNF-α levels was noted in the BIS 8 group relative to the BIS 2 and Cd groups, indicating a reduction at a higher dose. In microscopy, histopathological changes in the cardiac muscles of the BIS 8 group were evident compared to those of the Cd group. Conclusion BIS seemed to have protective effects against cardiac injury induced by cadmium and could be considered a novel therapeutic drug and prognostic biomarker in the pathology of the many cardiovascular diseases caused by heavy metal intake.

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Oxydative stress markers and cytokine levels in rosuvastatin-medicated hypercholesterolemia patients

Turkish Journal of Biochemistry ◽

10.1515/tjb-2018-0267 ◽

2018 ◽

Vol 44 (4) ◽

pp. 530-538

Author(s):

Aysun Çetin ◽

İhsan Çetin ◽

Semih Yılmaz ◽

Ahmet Şen ◽

Göktuğ Savaş ◽

...

Keyword(s):

Oxidative Stress ◽

Interleukin 1 ◽

Paraoxonase 1 ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Phenotypic Effect ◽

Necrosis Factor Alpha ◽

Stress Markers ◽

Tnf Α ◽

Before And After

Abstract Background Limited research is available concerning the relationship between oxidative stress and inflammation parameters, and simultaneously the effects of rosuvastatin on these markers in patients with hypercholesterolemia. We aimed to investigate the connection between cytokines and oxidative stress markers in patients with hypercholesterolemia before and after rosuvastatin treatment. Methods The study consisted of 30 hypercholesterolemic patients diagnosed with routine laboratory tests and 30 healthy participants. The lipid parameters, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), paraoxonase-1 (PON1) and malondialdehyde (MDA) levels in controls and patients with hypercholesterolemia before and after 12-week treatment with rosuvastatin (10 mg/kg/day), were analyzed by means of enzyme-linked immunosorbent assay. Results It was found that a 12-week cure with rosuvastatin resulted in substantial reductions in IL-1β, IL-6 and TNF-α and MDA levels as in rising activities of PON1 in patients with hypercholesterolemia. Before treatment, the PON1 levels were significantly negatively correlated with TNF-α and IL-6 in control group, while it was positively correlated with TNF-α in patients. Conclusion Our outcomes provide evidence of protected effect of rosuvastatin for inflammation and oxidative damage. It will be of great interest to determine whether the correlation between PON1 and cytokines has any phenotypic effect on PON1.

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Salidroside pretreatment protects against myocardial injury induced by heat stroke in mice

Journal of International Medical Research ◽

10.1177/0300060519868645 ◽

2019 ◽

Vol 47 (10) ◽

pp. 5229-5238

Author(s):

Guo-dong Chen ◽

Heng Fan ◽

Jian-Hua Zhu

Keyword(s):

Oxidative Stress ◽

Myocardial Injury ◽

Troponin I ◽

Heat Stroke ◽

Cardiac Injury ◽

Myocardial Damage ◽

Thiobarbituric Acid ◽

Protective Effects ◽

Creatine Kinase Mb ◽

Factor Α

Objective To explore the protective effects and mechanisms of salidroside on myocardial injury induced by heat stroke (HS) in mice. Methods We pretreated mice with salidroside for 1 week and then established an HS model by exposure to 41.2°C for 1 hour. We then examined the effects of salidroside on survival. We also assessed the severity of cardiac injury by pathology, and analyzed changes in levels of myocardial injury markers, inflammatory cytokines, and oxidative stress. Results Salidroside pretreatment significantly reduced HS-induced mortality and improved thermoregulatory function. Salidroside also provided significant protection against HS-induced myocardial damage, and decreased the expression levels of cardiac troponin I, creatine kinase-MB, and lactate dehydrogenase. Moreover, salidroside attenuated HS-induced changes in the inflammation markers tumor necrosis factor-α, interleukin (IL)-6, and IL-10, and down-regulated the oxidative stress response indicated by thiobarbituric acid reactant substances, malondialdehyde, reduced glutathione, and superoxide dismutase. Conclusions Salidroside pretreatment protected against HS-induced myocardial damage, potentially via a mechanism involving anti-inflammatory and anti-oxidative effects.

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Copper decreases gene expression of TNF-α, IL-10, and of matrix metalloproteinases MMP-2 and MMP-9 in isolated perfused rat livers

Biologia ◽

10.2478/s11756-007-0061-0 ◽

2007 ◽

Vol 62 (3) ◽

Cited By ~ 2

Author(s):

Albena Alexandrova ◽

Elena Bandžuchová ◽

Anton Kebis ◽

Marián Kukan ◽

Daniel Kuba

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Matrix Metalloproteinase ◽

Oxidative Dna Damage ◽

Interleukin 10 ◽

Matrix Metalloproteinase 2 ◽

Necrosis Factor Alpha ◽

Tissue Samples ◽

Tnf Α ◽

Rat Livers

AbstractCopper is known to induce oxidative stress in a number of models. It was shown that many pathophysiological events were associated with oxidative stress. Further, oxidative stress can increase gene expression of cytokines and of metalloproteinases. We previously found that copper toxic effects in isolated perfused rat livers were associated with significant oxidative stress (as assessed by lipid peroxidation, protein oxidation and oxidative DNA damage, particularly at concentration of 0.03 mM of Cu2+ in the perfusate). Here we investigated gene expression of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10); matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in frozen liver tissue samples by the real-time PCR assay. Compared to controls, copper at concentration of 0.01 mM did not affect gene expression of TNF-α, IL-10, MMP-2 and MMP-9, whereas copper at concentration of 0.03 mM significantly decreased gene expression of all the four TNF-α, IL-10, MMP-2 and MMP-9 by 69%, 81%, 43%, and 62%, respectively. These results suggest that copper-induced oxidative stress in the isolated rat liver can lead to the suppression of gene expression. Because TNF-α and metalloproteinases are involved also in liver regeneration, the suppression of these genes by copper may be one of the mechanisms by which acute intoxication of animals and humans with copper may impair regenerative capability of the liver.

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Antioxidant and Anti-Inflammatory Effects of Curcumin Nanoparticles on Drug-Induced Acute Myocardial Infarction in Diabetic Rats

Antioxidants ◽

10.3390/antiox8100504 ◽

2019 ◽

Vol 8 (10) ◽

pp. 504 ◽

Cited By ~ 9

Author(s):

Boarescu ◽

Bocșan ◽

Gheban ◽

Bulboacă ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Creatine Kinase ◽

Serum Levels ◽

Control Group ◽

Protective Effects ◽

Curcumin Nanoparticles ◽

Creatine Kinase Mb ◽

Anti Inflammatory

We have investigated the cardio-protective effects of pretreatment with curcumin nanoparticles (CUN) compared to conventional curcumin (CUS) on the changes in oxidative stress parameters and inflammatory cytokine levels during induced acute myocardial infarction (AMI) in rats with diabetes mellitus (DM). DM was induced with streptozotocin, and AMI with isoproterenol. Eight groups of seven Wister Bratislava rats were included in the study. The N-C was the normal control group, AMI-C was the group with AMI, DM-C was the group with DM, and DM-AMI-C was the group with DM and AMI. All four groups received saline solution orally during the whole experiment. S-DM-CUS-AMI and S-DM-CUN-AMI groups received saline for seven days prior to DM induction and continued with CUS (200 mg/kg bw, bw = body weight) for S-DM-CUS-AMI and CUN for S-DM-CUN-AMI (200 mg/kg bw) for 15 days before AMI induction. The CUS-DM-CUS-AMI group received CUS (200 mg/kg bw), while the CUN-DM-CUN-AMI received CUN (200 mg/kg bw) for seven days prior to DM induction, and both groups continued with administration in the same doses for 15 days before AMI induction. CUS and CUN prevented elevation of creatine kinase, creatine kinase-MB, lactate dehydrogenase in all groups, with better results in the CUN (S-DM-CUN-AMI and CUN-DM-CUN-AMI groups). CUS and CUN significantly reduced serum levels of oxidative stress markers (malondialdehyde, the indirect assessment of nitric oxide synthesis, and total oxidative status) and enhanced antioxidative markers (total antioxidative capacity and thiols, up to 2.5 times). All groups that received CUS or CUN showed significantly lower serum levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β. The best antioxidative and anti-inflammatory effects were obtained for the group that received CUN before DM induction (CUN-DM-CUN-AMI group). Pretreatment with CUN proved higher cardio-protective effects exerting an important antioxidative and anti-inflammatory impact in the case of AMI in DM.

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Effect of caraway on gentamicin-induced oxidative stress, inflammation and nephrotoxicity in rats

Veterinary Science Development ◽

10.4081/vsd.2015.5896 ◽

2015 ◽

Vol 5 (1) ◽

Cited By ~ 2

Author(s):

Hoda Erjaee ◽

Fatemeh Azma ◽

Saeed Nazifi

Keyword(s):

Oxidative Stress ◽

Inflammatory Cytokines ◽

Group Treatment ◽

Structural Damage ◽

Seed Oil ◽

Treated Group ◽

Control Group ◽

Protective Effects ◽

Simultaneous Treatment ◽

Tnf Α

Different potentially therapeutic approaches to prevent or attenuate gentamicin (GEM) induced nephrotoxicity have been proposed. The aim of the present study was to investigate the possible protective effects of caraway seed oil against GEM-induced nephrotoxicity in rats. Rats (24) were randomly assigned into four equal groups: i) normal control group, ii) treated with GEM, iii) pretreated with orally caraway seed oil 10 (mg kg−1) plus GEM and iv) treated with GEM and caraway seed oil 10 mg kg−1. Biochemical examinations were utilized for evaluation of the oxidative stress and renal nephrotoxicity. Creatinine, blood urea nitrogen (BUN), plasma malondialdehyde (MDA) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined. Administration of gentamicin to rats induced a marked renal failure, characterized by a significant increase in plasma creatinine and BUN concentrations. The animals treated with gentamicin alone showed a significantly higher plasma MDA level andlower SOD, GSH-Px and CAT activities when compared with the control group. Treatment and simultaneous treatment with caraway seed oil produced amelioration in MDA and increased the activity of antioxidant enzymes SOD, GSH-Px and CAT when compared with the gentamicin treated group. In addition, GEM nephrotoxicity increased renal inflammatory cytokines (TNF-α, IL-6 and IFN-γ). Pro-inflammatory cytokines were significantly decreased (P<0.05) in the test groups administered caraway seed oil. These findings suggest that caraway seed oil treatment attenuates renal dysfunction and structural damage through the reduction of oxidative stress and inflammation in rats.

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Anti-Oxidant and Anti-Inflammatory Effects of Lipopolysaccharide from Rhodobacter sphaeroides against Ethanol-Induced Liver and Kidney Toxicity in Experimental Rats

Molecules ◽

10.3390/molecules26247437 ◽

2021 ◽

Vol 26 (24) ◽

pp. 7437

Author(s):

Eman T. Mehanna ◽

Al-Shimaa A. Ali ◽

Fatma El-Shaarawy ◽

Noha M. Mesbah ◽

Dina M. Abo-Elmatty ◽

...

Keyword(s):

Rhodobacter Sphaeroides ◽

Iron Homeostasis ◽

Kidney Injury ◽

Control Group ◽

Protective Effects ◽

Necrosis Factor Alpha ◽

Hepcidin Expression ◽

Tnf Α ◽

Anti Oxidant ◽

Anti Inflammatory

This study aimed to investigate the protective effects of lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS) against ethanol-induced hepatotoxicity and nephrotoxicity in experimental rats. The study involved an intact control group, LPS-RS group, two groups were given ethanol (3 and 5 g/kg/day) for 28 days, and two other groups (LPS-RS + 3 g/kg ethanol) and (LPS-RS + 5 g/kg ethanol) received a daily dose of LPS-RS (800 μg/kg) before ethanol. Ethanol significantly increased the expression of nuclear factor kappa B (NF-κB) and levels of malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in the liver tissue and decreased anti-oxidant enzymes. Hepcidin expression was downregulated in the liver, with increased serum levels of ferritin and iron. Prior-administration of LPS-RS alleviated the increase in oxidative stress and inflammatory markers, and preserved iron homeostasis markers. In the kidney, administration of ethanol caused significant increase in the expression of NF-κB and the levels of TNF-α and kidney injury markers; whereas LPS-RS + ethanol groups had significantly lower levels of those parameters. In conclusion; this study reports anti-oxidant, anti-inflammatory and iron homeostasis regulatory effects of the toll-like receptor 4 (TLR4) antagonist LPS-RS against ethanol induced toxicity in both the liver and the kidney of experimental rats.

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Tangeretin Inhibits Oxidative Stress and Inflammation via Upregulating Nrf-2 Signaling Pathway in Collagen-Induced Arthritic Rats

Pharmacology ◽

10.1159/000501163 ◽

2019 ◽

Vol 104 (3-4) ◽

pp. 187-195 ◽

Cited By ~ 7

Author(s):

Xing Li ◽

Peigen Xie ◽

Yu Hou ◽

Shudong Chen ◽

Peiheng He ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Chinese Herb ◽

Biological Properties ◽

Therapeutic Effects ◽

Protective Effects ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Ifn Γ ◽

Anti Inflammatory

Background/Aims: Tangeretin (TAN), a major phytochemical in tangerine peels and an important Chinese herb, has multiple biological properties, especially antioxidative and anti-inflammatory effects. However, the mechanisms remain unclear. Based on these findings, the aim of the present study was to assess the antioxidant and anti-inflammatory properties of TAN in bovine type II collagen-induced arthritis rats. Methods: TAN (50 mg/kg) was given orally once daily for 14 days. The effects of treatment were evaluated by biochemical assay (articular elastase, myeloperoxidase, end products of lipid peroxidation [MDA], antioxidant enzyme, such as superoxide dismutase, catalase, glutathione), nitric oxide, and inflammatory cytokines (interleukin-1β [IL-1β], IL-10, tumor necrosis factor-alpha [TNF-α], interferon-γ [IFN-γ], and prostaglandin E2 [PGE2]). The protective effects of TAN against rheumatoid arthritis (RA) were evident from the decrease in arthritis scoring. Furthermore, the Nrf-2 signaling pathway was assessed to illustrate the molecular mechanism. Results: TAN had therapeutic effects on RA by decreasing the oxidative stress damage and regulating inflammatory cytokine expression, including suppression of the accumulation of MDA products, decreasing the IL-1β, TNF-α, IFN-γ, and PGE2 levels, enhancing the IL-10 and the activity of antioxidant enzymes, which was through upregulating Nrf-2 signaling pathway. Conclusion: TAN might have potential as a therapeutic agent for the treatment of RA.

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The Differences of Malondialdehyde Serum Level, Expression of Tumor Necrosis Factor Alpha and Vascular Endothelial Growth Factor, and the Area of Endometriotic Implants in Administration of Kebar Grass Extract (Biophytum petersianum) and Green Tea Extract (Camelia sinensis) to Mice

Majalah Obat Tradisional ◽

10.22146/mot.45237 ◽

2019 ◽

Vol 24 (3) ◽

pp. 169

Author(s):

Yuli Trisetiyono ◽

Noor Pramono ◽

Syarief Thaufik Hidayat ◽

Widjiati Widjiati

Keyword(s):

Oxidative Stress ◽

Serum Level ◽

Green Tea ◽

Green Tea Extract ◽

Control Group ◽

Vegf Expression ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Significant Difference ◽

Tea Extract

The pathological pathway of endometriosis remains unclear and involves complex etiologies. Increased oxidative stress is understood to be related to this disease. Oxidative stress produces reactive oxygen species, causes inflammation that is characterized by recruiting lymphocytes and phagocyte activation, produces cytokines that induce oxidation enzyme, and supports epithelium growth. Oxidative stress conjointly will increase angiogenesis and promotes the proliferation of endometriosis tissue within the peritoneal cavity. Kebar grass and green tea contain high antioxidants, are expected to extend antioxidant defense leading to reduced oxidative stress, inflammation, angiogenesis, and reduced endometriosis tissue implants. The objective is to analyze the consequences of Kebar grass and green tea extract to MDA serum level, TNF-α, and VEGF expression, and the area of the endometriotic implants in the mice models. The study was an experiment designed. It has been conducted within the Department of Obstetrics Gynecology, Faculty of Medicine Diponegoro University and Faculty of Veterinary Medicine Airlangga University. Twenty-one mice were divided into three groups, i.e., the first group of mouse models was given Kebar extract 3 mg/day; the second group was assigned green tea extract 1.1 mg/day; therefore the third group was a control group contains the untreated endometriosis mice. Each treatment was given for fourteen days. MDA serum level was measured by specto-photometric examination, the area of the endometriotic implants was measured by computer tracing technique, whereas TNF-α and VEGF expression of endometriotic implants were measured by IHC using Rammele Scale Index (ImmunoReactive Score). The MDA serum levels of the groups treated with Kebar grass extract and green tea extract were significantly lower than the control group (0.09±0.022 mmol, 0.07±0.019 mmol, and 0.30±0.062 mmol, respectively; p=0.001). TNF-α expression of the groups supplied with each treatment also lower than the control groups (2.43±1.521, 3.66±1.422, and 7.26±2.898, respectively; p=0.002). However, VEGF expression was not significantly different between Kebar grass extract group, green tea group, and the control (4.34±2.402, 4.57±1.998, 7.40±3.495, respectively; p=0.089). Finally, the area of the endometriotic implants of the mice models administered with all treatment was smaller than the control group (0.01±0.025 mm2, 8.76±18.776 mm2, and 34.80±13.079 mm2, respectively; p=0.003). Conclusion: Kebar grass extract, as well as green tea extract administration to endometriosis model mice, resulted in lower MDA serum level and TNF-α expression, smaller the area of endometriotic implants compared, but not resulted in a significant difference of VEGF expression.

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Antioxidant Herbs Supplementation Inhibits Endometriosis Extension in Mice

Journal of Biomedicine and Translational Research ◽

10.14710/jbtr.v5i2.4716 ◽

2019 ◽

Vol 5 (2) ◽

pp. 53-61

Author(s):

Yuli Trisetiyono ◽

Widjiati Widjiati ◽

Syarief Thaufik Hidayat ◽

Noor Pramono

Keyword(s):

Oxidative Stress ◽

Green Tea ◽

Cucumis Melo ◽

Serum Levels ◽

Green Tea Extract ◽

Control Group ◽

Vegf Expression ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Tea Extract

Background: Increased oxidative stress causes inflammation and increases angiogenesis. It presumed to promote the proliferation of endometriosis tissue. Kebar grass (Biophytum petersianum) and other herbs such as green tea and Cucumis melo, which contain high antioxidants, are expected to decrease oxidative stress, inflammation, angiogenesis, and reduced endometriosis implants.Objective: To investigate the effects of Kebar grass, green tea, and Cucumis melo to malondialdehyde serum, tumor necrosis factor alpha, and vascular endothelial growth factor expression, and the area of the endometriotic implants.Methods: Twenty-eight mice were divided into four groups, i.e., the first group of endometriosis mice was given Kebar grass extract; the second group was assigned green tea extract, the third group was given the combination of Cucumis melo extract–gliadin, and the last containing the untreated endometriosis mice as the control. Each treatment was given for 14 days. The data of MDA serum level, the area of the endometriotic implants, TNF-α, and VEGF expression were collected and analyzed.Results: The MDA serum levels of the groups treated with Kebar grass extract, green tea extract, and Cucumis melo extract – gliadin were significantly lower (p=0.001) than the control group. TNF-α expression of the groups provided with each treatment also lower than the control groups (p=0.002). However, only the administration of the Cucumis melo extract–gliadin resulted in lower VEGF expression compare with the control (p=0.017). Finally, the area of the endometriotic implants of the mice models administered with each treatment was smaller than the control group (p=0.003).Conclusion: Kebar grass as well as green tea and Cucumis melo–gliadin inhibits endometriotic implants extension by decreasing MDA serum and TNF-α expression.

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Molecular Evidence of the Inhibitory Potential of Melatonin against NaAsO2-Induced Aging in Male Rats

Molecules ◽

10.3390/molecules26216603 ◽

2021 ◽

Vol 26 (21) ◽

pp. 6603

Author(s):

Maryam Baeeri ◽

Tina Didari ◽

Madiha Khalid ◽

Solmaz Mohammadi-Nejad ◽

Seyed Mojtaba Daghighi ◽

...

Keyword(s):

Oxidative Stress ◽

Mrna Expression ◽

Tissue Injury ◽

High Mobility ◽

Male Rats ◽

Control Group ◽

Molecular Evidence ◽

Death Domain ◽

Tissue Samples ◽

Tnf Α

Arsenic (As) poisoning is widespread due to exposure to pollution. The toxic level of (As) causes oxidative stress-induced aging and tissue damage. Since melatonin (MLT) has anti-oxidant and anti-aging properties, we aimed to evaluate the protective effect of MLT against the toxicity of sodium arsenite (NaAsO2). Healthy male NMRI mice were divided into eight different groups. The control group received a standard regular diet. Other groups were treated with varying diets, including MLT alone, NaAsO2, and NaAsO2 plus MLT. After one month of treatment, biochemical and pathological tests were performed on blood, heart, and lung tissue samples. NaAsO2 increased the levels of TNF-α, 8-hydroxy-2-deoxy guanosine (8OHdG), malondialdehyde (MDA), reactive oxygen species (ROS), and high mobility group box 1 (HMGB1), increased the expression of TNF receptor type 1-associated death domain (TRADD) mRNA and telomerase reverse transcriptase, and decreased the expression of Klotho (KL) mRNA in both plasma and tissues. In contrast, MLT reduced MDA, ROS, HMGB1, lactate, and TNF-α enhanced the mRNA expression of KL, and suppressed the mRNA expression of the TERT and TRADD genes. Thus, MLT confers potent protection against NaAsO2- induced tissue injury and oxidative stress.

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