The Impact of Cnidoscolus aconitifolius (Linn)-Supplemented Diet on Cognitive Function, Oxidative stress and Histological changes in Wistar Rats

Introduction: Cognitive functions are defined as the mental processes through which information is received, processed, stored, and retrieved. Oxidation is considered as an important factor that affects negatively the brain function. The aim: To assess the impact of oxidative stress, as it is measured by oxidative markers or by the presence of anti-oxidants, on cognitive decline. Materials and methods: A systematic review of published observational studies in PubMed and in Scopus was performed. During the review process the keywords were used as follows: (“oxidative stress”) AND (“cognitive decline” OR “cognitive dysfunction” OR “cognitive impairment” OR “cognitive deficiency”) AND (“observational study” OR “cross sectional study” OR “prospective study” OR “retrospective study” OR “cohort study”). The search was conducted for the years from 2016 to 2020. Conclusions: Seventy-four eligible studies were identified. Thirteen studies met the inclusion and quality criteria and were included in the systematic review. The studies conducted in ten different countries. Information about oxidative stress biomarkers is available in eight studies, while information about antioxidant factors is in ten studies. In all the thirteen studies the cognitive function was assessed with specific tools – scales. In the majority of studies, the presence of high scores in oxidative markers was positively associated with cognitive decline, while higher levels of antioxidant markers were associated with better cognitive function. Our results indicate that oxidative stress may be significantly associated with cognitive decline. The presence of the antioxidants glutathione, uric acid, melatonin, cysteine and peroxide dismutase has a positive effect on cognitive function.

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Ovariectomy and its Antioxidative Effect on Bone

Volume 2: Biomedical and Biotechnology Engineering ◽

10.1115/imece2010-40581 ◽

2010 ◽

Author(s):

Durg V. Rai ◽

Harcharan Singh Ranu

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Free Radicals ◽

Bone Loss ◽

Wistar Rats ◽

Reactive Oxygen ◽

Oxygen Species ◽

Female Wistar Rats ◽

The Impact

Ovarian hormone deficiency increases the generation of reactive oxygen species. Oxidative stress due to reactive oxygen species (ROS) can cause oxidative damage to cells. Cells have a number of defense mechanisms to protect themselves from the toxicity of ROS. There is increasing evidence of the role of free radicals in bone resorption and bone loss. Ovariectomised female wistar rats had been used as the animal model for the study of osteoporosis. Even though, there are studies portraying the role of free radicals in bone loss, the defense mechanism adapted by bone in ovariectomised animals remains obscure. So, the impact of ovariectomy on the bone antioxidant system in rats was investigated. Twenty female wistar rats were taken and divided into two groups: ovariectomised and control. It had been found that a significant (p<0.001) decrease in the activity of various enzymes like CAT (catalase), SOD (superoxide dismutase) (p<0.001), GST (glutathione-s-transferase). However, an increase in the malondialdehyde levels was found to be 30% in the ovariectomised rats as compared to the controls. Thus the study elucidates the oxidative stress in bone under ovariectomy.

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Oxidative stress involvement in chronic chlorpyrifos-induced hepatocellular injury: Alleviating effect of vitamin C

Savannah Veterinary Journal ◽

10.36759/svj.2017.009 ◽

2018 ◽

pp. 1-9

Keyword(s):

Oxidative Stress ◽

Vitamin C ◽

Wistar Rats ◽

Liver Homogenate ◽

Hepatocellular Injury ◽

Histological Changes ◽

Male Wistar Rats ◽

Soya Oil ◽

Cholinergic Syndrome ◽

Glutamyl Transferase

Introduction: Chlorpyrifos (CPF), a phosphorothionate chlorinated organophosphate (OP) insecticide is widely used in agriculture and public health. Like other OP insecticides, its main mechanism of toxicity is the inhibition of acetylcholinesterase (AChE) leading to cholinergic syndrome. Since toxicity occurs at doses that do not inhibit AChE or long after its restoration, other mechanisms including the induction of oxidative stress have been widely implicated. The present study was aimed at evaluating the mitigating effect of vitamin C on CPF-induced hepatocellular injury in Wistar rats. Methods: Twenty adult male Wistar rats were divided into 4 groups of five animals in each group. The four groups were exposed by gavage to soya oil (2 ml/kg), vitamin C (100 mg/kg), CPF (10.6 mg/kg~1/8th LD50) and vitamin C (100 mg/kg) + CPF (10.6 mg/kg; 30 min later), respectively for 17 weeks. The sera obtained from blood samples collected from the animals were analysed for the levels of total proteins, albumin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), g-glutamyl transferase (GGT) while globulin concentration and albumin/globulin ratio were calculated. The liver homogenate was evaluated for the levels of malonaldehyde (MDA), superoxide dismutase (SOD) and catalase (CAT), and histological changes. Results: The study showed that CPF altered the levels of the serum hepatic enzymes, hepatic MDA SOD and CAT, in addition to inducing hepatocellular degeneration. All these parameters were alleviated by pretreatment with vitamin C. Significance: CPF-induced hepatocellular injury which was partly due to oxidative changes was mitigated by vitamin C partly due to its antioxidative activity.

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Quercetin Effects on Hepatotoxicity Induced by Titanium Dioxide Nanoparticles in Rats

Jundishapur Journal of Natural Pharmaceutical Products ◽

10.5812/jjnpp.83523 ◽

2019 ◽

Vol 15 (3) ◽

Author(s):

Maryam Shirani ◽

Layasadat Khorsandi ◽

Hadis Alidadi

Keyword(s):

Oxidative Stress ◽

Titanium Dioxide ◽

Wistar Rats ◽

Titanium Dioxide Nanoparticles ◽

Serum Biomarker ◽

Histological Changes ◽

Nuclear Pyknosis ◽

Female Wistar Rats ◽

Body Organ ◽

Induced Apoptosis

Background: Most nanoparticles have adverse impacts on the liver, which is a vital body organ, by the induction of oxidative stress. Objectives: This study was designed to evaluate the hepatoprotective effects of quercetin (QCT) against the toxicity of nanoscale titanium dioxide (NTiO2) in Wistar rats. Methods: The present study was conducted on 32 adult female Wistar rats assigned into 4 groups of control, NTiO2 (50 mg/kg), NTiO2 + Quercetin (50 + 75 mg/kg), and Quercetin (75 mg/kg). The animals exposed to NTiO2 were administered by 50 mg/kg of NTiO2 for 21 days. The Quercetin + NTiO2 rats received Quercetin before exposing to NTiO2 for 7 days. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) of serum were considered indicators of the hepatotoxicity. The oxidative stress was assessed by measuring the activity of catalase (CAT) and superoxide dismutase (SOD) as well as the level of malondialdehyde (MDA) in the liver. TUNEL assay and histological changes were also assessed. Results: The NTiO2 significantly elevated the MDA level (P < 0.01), enhanced the serum biomarker levels, reduced the CAT (P < 0.01) and SOD (P < 0.01) activities. The NTiO2 also aggregated the red blood cells, and caused inflammatory cell infiltration, nuclear pyknosis and fat deposit in hepatocytes, as well as induced apoptosis in the liver tissue. Pretreatment with QCT quenched oxidative stress, attenuated the histological changes, elevated the CAT (P < 0.01) and SOD (P < 0.01) activities, normalized the serum biomarker levels and decreased apoptosis (P < 0.001). Conclusions: The QCT has an inhibitory impact on hepatotoxicity induced by nanoparticles in rats.

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RALBP1 in Oxidative Stress and Mitochondrial Dysfunction in Alzheimer’s Disease

Cells ◽

10.3390/cells10113113 ◽

2021 ◽

Vol 10 (11) ◽

pp. 3113

Author(s):

Sanjay Awasthi ◽

Ashly Hindle ◽

Neha A. Sawant ◽

Mathew George ◽

Murali Vijayan ◽

...

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cognitive Function ◽

Mitochondrial Dysfunction ◽

Mitochondrial Function ◽

Gene Networks ◽

Sensory Function ◽

Expression Of Genes ◽

The Impact

The purpose of our study is to understand the role of the RALBP1 gene in oxidative stress (OS), mitochondrial dysfunction and cognition in Alzheimer’s disease (AD) pathogenesis. The RALPB1 gene encodes the 76 kDa protein RLIP76 (Rlip). Rlip functions as a stress-responsive/protective transporter of glutathione conjugates (GS-E) and xenobiotic toxins. We hypothesized that Rlip may play an important role in maintaining cognitive function. The aim of this study is to determine whether Rlip deficiency in mice is associated with AD-like cognitive and mitochondrial dysfunction. Brain tissue obtained from cohorts of wildtype (WT) and Rlip+/− mice were analyzed for OS markers, expression of genes that regulate mitochondrial fission/fusion, and synaptic integrity. We also examined mitochondrial ultrastructure in brains obtained from these mice and further analyzed the impact of Rlip deficiency on gene networks of AD, aging, stress response, mitochondrial function, and CREB signaling. Our studies revealed a significant increase in the levels of OS markers and alterations in the expression of genes and proteins involved in mitochondrial biogenesis, dynamics and synapses in brain tissues from these mice. Furthermore, we compared the cognitive function of WT and Rlip+/− mice. Behavioral, basic motor and sensory function tests in Rlip+/− mice revealed cognitive decline, similar to AD. Gene network analysis indicated dysregulation of stress-activated gene expression, mitochondrial function and CREB signaling genes in the Rlip+/− mouse brain. Our results suggest that Rlip deficiency-associated increases in OS and mitochondrial dysfunction could contribute to the development or progression of OS-related AD processes.

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Involvement of SIRT1-eNOS Axis in Vascular Senescence Responses to Ursolic Acid and Exercise Training in Aged Type 2 Diabetes Model of Rats

10.21203/rs.3.rs-631236/v1 ◽

2021 ◽

Author(s):

Masume Kazemi Pordanjani ◽

Ebrahim Banitalebi ◽

Mehrdad Roghani ◽

Roohullah Hemmati

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Type 2 Diabetes ◽

Endurance Training ◽

Ursolic Acid ◽

Wistar Rats ◽

Vascular Aging ◽

Male Wistar Rats ◽

The Impact

Abstract Background Ursolic acid (UA) mediates the vasorelaxant activity via nitric oxide (NO) release, and up-regulation of eNOS in endothelial cells in disease conditions with increased oxidative stress. The present study aimed to reflect on the impact of eight weeks of a combination of ursolic acid (UA) supplementation and resistance/endurance training in old male Wistar rats having high-fat diet and/or low-dose streptozotocin-induced type 2 diabetes (HFD/STZ-induced T2D), with an emphasis on sirtuin 1 (SIRT1)-endothelial nitric oxide synthase (eNOS) axis and oxidative stress (OS) indices in their aortic tissues. Methods A total number of 56 21-month-old male Wistar rats with HFD/STZ-induced T2Dwere randomized into seven groups (n = eight animals per group): (1) sedentary old non-diabetic (C); (2) sedentary HFD/STZ-induced T2D (D); (3) sedentary HFD/STZ-induced T2D plus UA (UA) (DU); (4) endurance-trained HFD/STZ-induced T2D (DE); (5) resistance-trained HFD/STZ-induced T2D (DR); (6) endurance-trained HFD/STZ-induced T2D plus UA (DEU); and (7) resistance-trained STZ-diabetic plus UA (DRU) rats. Results The study results established no significant interaction between the UA supplementation and the resistance/endurance training with regard to the levels of glucose (p = 0.534), insulin (p = 0.327), high-density lipoprotein cholesterol (HDL-c) (p = 0.960), cholesterol (p = 0.107), SIRT1 (p = 0.640), and eNOS (p = 0.151). However, the resistance/endurance training plus the UA consumption could partially reverse the levels of malondialdehyde (MDA) (p = 0.001), nitric oxide (NO) (p = 0.009), as well as total antioxidant capacity (TAC) (p = 0.016). Conclusions In general, the UA supplementation combined with the resistance/endurance training did not affect vascular aging biomarkers. To develop novel practical nutritional strategies involving UA intake, further studies are thus needed to clarify how chronic consumption of UA with/without resistance/endurance training reverses vascular aging process in old male Wistar rats with HFD/STZ-induced T2D.

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Preventive effect of Caralluma fimbriata against high-fat diet induced injury to heart by modulation of tissue lipids, oxidative stress and histological changes in Wistar rats

Archives of Physiology and Biochemistry ◽

10.1080/13813455.2019.1693601 ◽

2019 ◽

pp. 1-9

Author(s):

Sudhakara Gujjala ◽

Mallaiah Putakala ◽

Sasi Bhusana Rao Bongu ◽

Rajendran Ramaswamy ◽

Saralakumari Desireddy

Keyword(s):

Oxidative Stress ◽

High Fat Diet ◽

Wistar Rats ◽

Preventive Effect ◽

High Fat ◽

Histological Changes ◽

Tissue Lipids

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Effects of Leaf Extract of Cnidoscolus aconitifolius on Serum Lipids and Oxidative Stress Markers of Male Wistar Rats

Asian Journal of Biochemistry, Genetics and Molecular Biology ◽

10.9734/ajbgmb/2020/v5i130120 ◽

2020 ◽

pp. 47-52

Author(s):

Ijeoma Ezebuiro ◽

Chibuike Obiandu ◽

Friday Saronee ◽

Adesua C. Obiandu

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

Density Lipoprotein ◽

Lipoprotein Cholesterol ◽

Oxidative Stress Markers ◽

Stress Markers ◽

Cnidoscolus Aconitifolius ◽

Significant Difference ◽

Male Wistar Rats ◽

And Oxidative Stress

Introduction: Cnidoscolus aconitifolius is considered to be an important and effective medicinal plant in folklore remedies where it has been applied as an alternative therapy for the treatment of various ailments. Aim: The present study aims to determine the effects of Cnidoscolus aconitifolius on lipid profile and some oxidative stress markers of male Wistar rats. Methodology: A total of 15 male wistar rats were procured for the study and randomly assigned into three groups of 5 rats each. Group 1 served as control and received distilled water only. Group 2 received 200 mg/kg and group 3 received 400mg/kg of the hydromethanolic (1:4) extract of Cnidoscolus aconitifolius which was administered as single daily dose using oral cannula. On completion of treatment, blood samples were collected by cardiac puncture for determination of some serum lipid parameters and oxidative stress markers. Results: Results showed that there were no significant difference in the serum level of total cholesterol, triglyceride, low density lipoprotein cholesterol and high density lipoprotein cholesterol at both doses of the extract, compared to control. However, compared to control, there was a significant (p<0.05) increase in the activity of superoxide dismutase and glutathione reductase but significant reduction in malondialdehyde level. The catalase enzyme activity was not significant. Conclusion: The result obtained suggest that the extract may be useful in reducing oxidative stress by improving some antioxidant enzyme activities and may also prevent cell death due to lipid peroxidation.

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