scholarly journals Effect of cyclophosphamide on hematological and physiological and possible protective role of Berberis vulgaris in mice

2021 ◽  
pp. 1-7
Author(s):  
Idriss H. Mohamed
Keyword(s):  
Oxidative Stress ◽  
White Blood Cells ◽  
Protective Role ◽  
Physiological Parameters ◽  
Protective Effects ◽  
Distribution Width ◽  
Lung Cancers ◽  
Berberis Vulgaris ◽  
Anti Cancer ◽  
Hematological And Biochemical Parameters

Aim of study to investigate the effect of certain natural products from medicinal plants as adjuvant systems to reduce toxicity of chemotherapy. cyclophosphamide (CTX) is anti-cancer DNA alkylating chemotherapeutic agent to act against a variety of tumors in head and neck, testicular, ovarian, bladder, small-cell lung cancers, this study performed to investigate the effect of Berberis vulgaris in combination with CTX on hematological and physiological parameters induced by CTX in mice. In this study we evaluate the possible protective effects of Berberis vulgaris on hematological and physiological parameters in mice chronically treated with CTX. Four groups of mice were examined: a control (I), mice treated with CTX (II), mice treated with CTX + Berberis vulgaris (III), and mice treated with Berberis vulgaris (IV). All animals were treated for successively 5 days and killed one week after the last treatment, The results show significant decreases in levels of red blood cell distribution width (RDW), white blood cells (WBCs), neutrophils and lymphocytes counts with increases in levels of monocytes. Also, hepatocytes oxidative stress which characterized by significant increases in the serum activities aspartate aminotransferase (AST), alanine aminotransferase (ALT). Berberis vulgaris combined with CTX or Berberis vulgaris alone successfully normalized the hematological and biochemical parameters in form returning (RDW), (WBCs), monocytes and lymphocytes count to normal level. Hepatocytes oxidative stress, which characterized by a significant decrease in the serum activities of (AST) and (ALT). Keywords: Cyclophosphamide; Berberis vulgaris; Lymphocytes; Hepatocytes; Significant

scholarly journals Fucoidan Protects against Acute Sulfoxaflor-Induced Hematological/Biochemical Alterations and Oxidative Stress in Male Mice

2021 ◽  
Vol 15 (1) ◽  
pp. 16
Author(s):  
Petek Piner Benli ◽  
Merve Kaya ◽  
Yusuf Kenan Dağlıoğlu
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Biological Activities ◽  
Hematological Parameters ◽  
Sulfated Polysaccharide ◽  
Protective Role ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Hematological And Biochemical Parameters ◽  
And Oxidative Stress

Fucoidan is a sulfated polysaccharide which can be found among a number of macroalgea species. It has a broad spectrum of biological activities including anti-oxidant, anti-tumor, immunoregulation, anti-viral and anti-coagulant. The current study was performed to investigate possible protective effects of fucoidan for sulfoxaflor-induced hematological/biochemical alterations and oxidative stress in the blood of male Swiss albino mice. For this purpose, sulfoxaflor was administered at a dose of 15 mg/kg/day (1/50 oral LD50), and fucoidan was administered at a dose of 50 mg/kg/day by oral gavage alone and combined for 24 h and 7 days. Hematological parameters (RBC, HGB, HCT, MCV, MCH, MCHC, Plt, WBC, Neu, Lym and Mon), serum biochemical parameters (AST, ALT, GGT, LDH, BUN, Cre and TBil), and serum oxidative stress/antioxidant markers (8-OHdG, MDA, POC and GSH) were analyzed. The results indicated that sulfoxaflor altered hematological and biochemical parameters and caused oxidative stress in mice; fucoidan ameliorated some hematological and biochemical parameters and exhibited a protective role as an antioxidant against sulfoxaflor-induced oxidative stress.

scholarly journals Protection against Doxorubicin-Induced Cytotoxicity by Geniposide Involves AMPKα Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Yan-Yan Meng ◽  
Yu-Pei Yuan ◽  
Xin Zhang ◽  
Chun-Yan Kong ◽  
Peng Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Potential ◽  
Cell Loss ◽  
Protective Role ◽  
Protective Effects ◽  
Morphological Examination ◽  
Heart Injury ◽  
Amp Activated Protein Kinase

Oxidative stress and cardiomyocyte apoptosis play critical roles in the development of doxorubicin- (DOX-) induced cardiotoxicity. Our previous study found that geniposide (GE) could inhibit cardiac oxidative stress and apoptosis of cardiomyocytes but its role in DOX-induced heart injury remains unknown. Our study is aimed at investigating whether GE could protect against DOX-induced heart injury. The mice were subjected to a single intraperitoneal injection of DOX (15 mg/kg) to induce cardiomyopathy model. To explore the protective effects, GE was orally given for 10 days. The morphological examination and biochemical analysis were used to evaluate the effects of GE. H9C2 cells were used to verify the protective role of GE in vitro. GE treatment alleviated heart dysfunction and attenuated cardiac oxidative stress and cell loss induced by DOX in vivo and in vitro. GE could activate AMP-activated protein kinase α (AMPKα) in vivo and in vitro. Moreover, inhibition of AMPKα could abolish the protective effects of GE against DOX-induced oxidative stress and apoptosis. GE could protect against DOX-induced heart injury via activation of AMPKα. GE has therapeutic potential for the treatment of DOX cardiotoxicity.

scholarly journals The Protective Role of Antioxidants in the Defence against ROS/RNS-Mediated Environmental Pollution

2014 ◽  
Vol 2014 ◽  
pp. 1-22 ◽  
Author(s):  
Borut Poljšak ◽  
Rok Fink
Keyword(s):  
Oxidative Stress ◽  
Nitrosative Stress ◽  
Environmental Pollutants ◽  
Protective Role ◽  
Age Related Macular Degeneration ◽  
Protective Effects ◽  
Age Related ◽  
Dietary Antioxidant ◽  
Polycyclic Aromatic ◽  
Antioxidant Supplements

Overproduction of reactive oxygen and nitrogen species can result from exposure to environmental pollutants, such as ionising and nonionising radiation, ultraviolet radiation, elevated concentrations of ozone, nitrogen oxides, sulphur dioxide, cigarette smoke, asbestos, particulate matter, pesticides, dioxins and furans, polycyclic aromatic hydrocarbons, and many other compounds present in the environment. It appears that increased oxidative/nitrosative stress is often neglected mechanism by which environmental pollutants affect human health. Oxidation of and oxidative damage to cellular components and biomolecules have been suggested to be involved in the aetiology of several chronic diseases, including cancer, cardiovascular disease, cataracts, age-related macular degeneration, and aging. Several studies have demonstrated that the human body can alleviate oxidative stress using exogenous antioxidants. However, not all dietary antioxidant supplements display protective effects, for example,β-carotene for lung cancer prevention in smokers or tocopherols for photooxidative stress. In this review, we explore the increases in oxidative stress caused by exposure to environmental pollutants and the protective effects of antioxidants.

Role of PI3K/AKT/mTOR Pathway Associated Oxidative Stress and Cardiac Dysfunction in Takotsubo Syndrome

2020 ◽  
Vol 17 (1) ◽  
pp. 35-43
Author(s):  
Shan Mao ◽  
Xianghong Luo ◽  
Yu Li ◽  
Chaorong He ◽  
Fuhua Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Myocardial Dysfunction ◽  
Cardiac Injury ◽  
Protective Role ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Protective Effects ◽  
Takotsubo Syndrome ◽  
Akt Inhibitor

Introduction: Takotsubo syndrome (TTS) is a stress-induced cardiomyopathy, but the accurate cause of this syndrome is still unknown. Methods: β-adrenergic agonist isoproterenol (ISO) is used to establish the TTS rats model. TTS rats were treated with or without LY294002 or Rapamycin. The rat cardiomyoblast cell line H9C2 was subjected to infect with constitutively active Akt (myr-Akt) or dominant-negative mutant Akt (dn-Akt) and then, treated with ISO. Cell apoptosis was assessed using the Bax/ Bcl-2 ratio. In addition, reactive oxygen species (ROS) levels were measured using dihydroethidium (DHE). Mitochondrial superoxide generation and membrane potential were assayed by MitoSOX and JC-1 fluorescence intensity. Results: ISO might induce the erratic acute cardiac dysfunction and overexpression of PI3K/AKT/mTOR. Moreover, it also increased the oxidative stress and apoptosis in TTS rats. The Akt inhibitor significantly reversed the cardiac injury effect, which triggered by ISO treatment. In H9C2 cells, the inhibition of Akt provides a protective role against ISO-induced injury by reducing oxidative stress, apoptosis and mitochondrial dysfunction. Conclusion: This study provided new insight into the protective effects of myocardial dysfunction in TTS rats via chronic inhibition of the PI3K/AKT/mTOR expression, which could reduce mitochondrial ROS and oxidative stress-induced apoptosis. PI3K/AKT/mTOR inhibitor could be a therapeutic target to treat cardiovascular dysfunction induced by stress cardiomyopathy.

scholarly journals Sirt1 Inhibits Oxidative Stress in Vascular Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Weijin Zhang ◽  
Qiaobing Huang ◽  
Zhenhua Zeng ◽  
Jie Wu ◽  
Yaoyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Key Factor ◽  
Antioxidative Stress

The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF-κB, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.

scholarly journals Pharmacological and biochemical studies on the protective effects of melatonin during stress-induced behavioral and immunological changes in relation to oxidative stress in rats

2016 ◽  
Vol 94 (3) ◽  
pp. 296-301 ◽  
Author(s):  
Rishi Pal ◽  
Kavita Gulati ◽  
B.D. Banerjee ◽  
Arunabha Ray
Keyword(s):  
Oxidative Stress ◽  
Brain Homogenate ◽  
Protective Role ◽  
Dependent Manner ◽  
Protective Effects ◽  
Immunological Parameters ◽  
Stress Markers ◽  
Test Parameters ◽  
Neuropsychiatric Diseases ◽  
Immunological Changes

Stress is known to precipitate neuropsychiatric diseases, and depending upon its nature and intensity it can also influence the functioning of the immune system. Melatonin (N-acetyl-5-methoxy tryptamine) a pineal gland hormone and potent antioxidant is known to protect against many diseases. Effect of melatonin in stress-induced neuro-immunomodulation is not well elucidated. Therefore in the present study, the protective effects of melatonin were evaluated in restraint stress (RS)-induced behavioral and immunological changes in rats. RS for 1 h significantly reduces (i) percentage of open-arm entries and (ii) percentage of time spent on open-arm in elevated plus maze (EPM) test parameters (p < 0.01) and significant increase in MDA levels in brain homogenate when compared to non-RS control groups (p < 0.05). In immunological studies, both humoral and cell-mediated immune responses to antigen were significantly suppressed by RS for 1 h for 5 consecutive days, as evidenced by significant reduction in (i) anti-SRBC antibody titre, (ii) PFC counts, (iii) percentage change in paw volume, and (iv) Th1 (IFN-γ) and Th2 (IL-4) cytokine levels (p < 0.001 in all parameters). These RS-induced immunological changes were associated with significantly increased lipid peroxidation (MDA) levels in serum and significantly decreased activity of (i) SOD, (ii) CAT, and (iii) GSH levels in RS (X5)-exposed group (p < 0.02). Pretreatment with melatonin (10, 50, and 100 mg/kg) significantly reversed these RS-induced changes in EPM test parameters and humoral and cell-mediated immunological parameters, as well as oxidative stress markers in a dose-dependent manner by differential degrees (p < 0.001). Results are strongly suggestive of the involvement of free radicals during stress-induced neurobehavioral and immunological changes. These changes were significantly restored by melatonin pretreatment. We can conclude that melatonin may have a protective role during such stress-induced neuro-immunomodulation.

scholarly journals Roundup-induced biochemical and histopathological changes in the liver and kidney of rats: the ameliorative effects of Linum usitatissimum oil

2020 ◽  
Author(s):  
Nesrine Djaber ◽  
Lynda Sabrina Ounaceur ◽  
Baya Nouha Moubine ◽  
Taha Khaldi ◽  
Mereim Rouag ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Linum Usitatissimum ◽  
Protective Role ◽  
Control Group ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Antioxidant Power ◽  
Renal Markers ◽  
Ferric Reducing Antioxidant Power ◽  
Liver And Kidney

The present study was undertaken to evaluate the protective effects of Linum usitatissimum oil (LuO) against sub-chronic Roundup (RDP)-induced toxicity and oxidative stress in rats. Rats were divided into four groups: control group (no treatment), RDP group (Roundup at 269.9 mg/kg b.w.), LuO group (0.5 g/kg b.w. of LuO) and RDP+LuO group (RDP and LuO simultaneously). LuO decreased the ferric reducing antioxidant power (FRAP) (IC50=10.36 μg/ml) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) (IC50=22.85 mg/ml) in the tested tissues. The 30-day exposure of rats to RDP caused an increase in serum hepatic and renal markers: AST, ALT, ALP, LDH, γGT, bilirubin, urea, and creatinine. In addition, SOD, CAT and GST activities decreased by 43%, 61%, and 61%, respectively, while GPx activity, MDA and PCOs levels increased by 80%, 46%, 25%, respectively. LuO treatment alleviated hepatotoxicity in RDP-treated rats, showing improved levels of oxidative stress biomarkers and plasma biochemical parameters. The histological examination of the liver and kidney confirmed the changes in Roundup-treated rats and demonstrated the protective role of LuO.

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.

Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E

2009 ◽  
Vol 34 (2) ◽  
pp. 124-135 ◽  
Author(s):  
Subhasis Das ◽  
N. Gautam ◽  
Sankar Kumar Dey ◽  
Tarasankar Maiti ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Body Mass ◽  
Brain Mitochondria ◽  
Brain Regions ◽  
Protective Role ◽  
Andrographis Paniculata ◽  
Protective Effects ◽  
The Brain

Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg·kg body mass–1·day–1) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg·kg body mass–1·day–1); and vitamin E (50 mg·kg body mass–1·day–1) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito–ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito–ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.

scholarly journals Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α2-Adrenergic Receptor-Dependent Suppression of Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Peibiao Lv ◽  
Tufeng Chen ◽  
Peibin Liu ◽  
Lei Zheng ◽  
Jingling Tian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Orthotopic Liver Transplantation ◽  
Adrenergic Receptor ◽  
Protective Role ◽  
Intestinal Injury ◽  
Protective Effects ◽  
Barrier Dysfunction

Patients with orthotopic liver transplantation (OLT) frequently develop acute gut injury (AGI), and dexmedetomidine (Dex) has been reported to exert a protective effect against AGI. We investigated whether Dex protects against AGI through antioxidative stress effects by the Nrf2/HO-1 antioxidative signaling pathway. Rats were randomly allocated into a sham group and six orthotopic autologous liver transplantation (OALT) groups receiving different doses of Dex together with/without α2-adrenergic receptor (AR) blockers. Intestinal tissues were collected to visualize the barrier damage and to measure the indexes of oxidative stress. For in vitro studies, rat intestinal recess epithelial cells (IEC-6) underwent hypoxia/reoxygenation (H/R), and the protective role of Dex was evaluated after α2A-AR siRNA silencing. OALT resulted in increased oxidative stress, significant intestinal injury, and barrier dysfunction. Dex attenuated OALT-induced oxidative stress and intestinal injury, which was abolished by the pretreatment with the nonspecific α2A-AR siRNA blocker atipamezole and the specific α2A-AR siRNA blocker BRL-44408, but not by the specific 2B/C-AR siRNA blocker ARC239. Silencing of α2A-AR siRNA also attenuated the protective role of Dex on alleviating oxidative stress in IEC-6 cells subjected to H/R. Dex exerted its protective effects by activating Nrf2/HO-1 antioxidative signaling. Collectively, Dex attenuates OALT-induced AGI via α2A-AR-dependent suppression of oxidative stress, which might be a novel potential therapeutic target for OALT-induced AGI.

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