Effect of atherosclerosis and the protective effect of the antioxidant vitamin E on the rabbit cerebellum

Microscopy ◽  
2019 ◽  
Vol 68 (5) ◽  
pp. 369-378 ◽  
Author(s):  
Maha Abdel Fatah Elbeltagy ◽  
Wael Badr Elkholy ◽  
Ahmed Said Salman
Keyword(s):  
Vitamin E ◽  
Caspase 3 ◽  
Molecular Layer ◽  
Protective Role ◽  
Diet Group ◽  
Fine Motor ◽  
Antioxidant Vitamin ◽  
Group I ◽  
Ordinary Diet

Abstract Background Atherosclerosis is a major cardiovascular disease and one of the commonest causes of mortality in the world. Speech, balance, fine motor control and cognition are affected by atherosclerosis of cerebellar arteries. This study investigated the protective role of vitamin E against induced atherosclerosis in the rabbit cerebellum. Materials and methods Forty Rex New Zealand adult male rabbits were randomly divided into four groups (10 rabbits each). Group I was designated as the control and received an ordinary diet. Group II received an ordinary diet, but with vitamin E (12 mg/kg/day) added. Group III were given an ordinary diet along with 1% cholesterol powder for 6 weeks. Finally, group IV received an ordinary diet with both 1% cholesterol powder and vitamin E (12 mg/kg/day). Cerebellum samples were stained with haematoxylin and eosin and examined using light microscopy, along with quantitative immunohistochemical assessments of the expression of caspase-3, glial fibrillary acidic protein (GFAP) and inducible nitric oxide synthase (iNOS). Results Cerebellum sections from cholesterol-treated rabbits showed ischaemic changes as fibre density decreased, with vacuolation of the molecular layer, and deformed and shrunken Purkinje cells. A significant increase in caspase-3, GFAP and iNOS immunoreactivity was found. However, vitamin E administration reduced these ischaemic manifestations. Conclusions The results demonstrate the neurological protective role of vitamin E therapy in atherosclerosis.

scholarly journals The Protective Role of Prenatal Alpha Lipoic Acid Supplementation against Pancreatic Oxidative Damage in Offspring of Valproic Acid-Treated Rats: Histological and Molecular Study

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 239
Author(s):  
Fatma M. Ghoneim ◽  
Hani Alrefai ◽  
Ayman Z. Elsamanoudy ◽  
Salwa M. Abo El-khair ◽  
Hanaa A. Khalaf
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Lipoic Acid ◽  
Caspase 3 ◽  
Protective Role ◽  
Alpha Lipoic Acid ◽  
Group Iii ◽  
Rat Offspring ◽  
Group I

Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and β cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

scholarly journals Protective role of antioxidant vitamin E and catechin on idarubicin-induced cardiotoxicity in rats

2002 ◽  
Vol 35 (11) ◽  
pp. 1379-1387 ◽  
Author(s):  
S. Kalender ◽  
Y. Kalender ◽  
A. Ates ◽  
M. Yel ◽  
E. Olcay ◽  
...  
Keyword(s):  
Vitamin E ◽  
Protective Role ◽  
Antioxidant Vitamin

Genoprotective role of vitamin E and selenium in rabbits anaesthetized with sevoflurane

2004 ◽  
Vol 23 (8) ◽  
pp. 413-419 ◽  
Author(s):  
Cetin Kaymak ◽  
Ela Kadioglu ◽  
Hulya Basar ◽  
Semra Sardas
Keyword(s):  
Dna Damage ◽  
Vitamin E ◽  
Comet Assay ◽  
Antioxidant Supplementation ◽  
Group Iii ◽  
Sevoflurane Anaesthesia ◽  
Group I ◽  
The Mean ◽  
Group Ii

In this study, genotoxic effects of repeated sevoflurane anaesthesia were investigated in rabbits with or without antioxidant supplementation. Twenty-one New Zealand male rabbits were included in the study and randomized into three groups as: placebo treated (Group I), vitamin E supplemented (Group II) and selenium supplemented (Group III). Vitamin E and selenium were given intraperitoneally for 15 days before anaesthesia treatment. Anaesthesia was administered using 3% sevoflurane in 4 L/min oxygen for a 3-hour period and continued for 3 days. Blood samples were collected before anaesthesia (Sample 1), after the first, second and third days of sevoflurane administration (Sample 2, Sample 3 and Sample 4 respectively) and the last samples were taken 5 days after the last sevoflurane administration (Sample 5). Genotoxic damage was examined using the comet assay. The degree of damage is assessed by grading the cells into three categories of no migration (NM), low migration (LM) and high migration (HM) depending on the fraction of DNA pulled out into the tail under the influence of the electric field. The number of comets in each sample was calculated (1 × number of comets in category NM + 2 × number of comets in category LM + 3 ×number of comets in category HM) and expressed as the total comet score (TCS), which summarizes the damage frequencies. In Group I, a significant increase in the mean TCSs was observed for Samples 3 and 4 as compared with Sample 1. However, there were no significant differences between Samples 1, 2 and 5. The mean TCS of Sample 4 was significantly higher than Sample 1, 2 and 3 in Group II. Group III demonstrated no significant mean TCSs for any experimental conditions. Statistical differences were also observed between the groups with significant P values. This experimental study points out the presence of DNA damage with repeated sevoflurane anaesthesia and the genoprotective role of antioxidant supplementation on DNA damage in mononuclear leukocytes of rabbits by highly sensitive comet assay.

scholarly journals Differential role of SIRT1/MAPK pathway during cerebral ischemia in rats and humans

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sireesh Kumar Teertam ◽  
Phanithi Prakash Babu
Keyword(s):  
Cerebral Ischemia ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Protective Role ◽  
Akt Signaling ◽  
Sirtuin 1 ◽  
Neurological Dysfunction ◽  
Dependent Manner ◽  
Erk Mapk

AbstractCerebral ischemia (CI) is a severe cause of neurological dysfunction and mortality. Sirtuin-1 (Silent information regulator family protein 1, SIRT1), an oxidized nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, plays an important role in protection against several neurodegenerative disorders. The present study aims to investigate the protective role of SIRT1 after CI in experimental young and aged rats and humans. Also, the study examines the possible regulatory mechanisms of neuronal death in CI settings. Immunoblotting and immunohistochemistry were used to evaluate changes in the expression of SIRT1, JNK/ERK/MAPK/AKT signaling, and pro-apoptotic caspase-3 in experimental rats and CI patients. The study findings demonstrated that, in aged experimental rats, SIRT1 activation positively influenced JNK and ERK phosphorylation and modulated neuronal survival in AKT-dependent manner. Further, the protection conferred by SIRT1 was effectively reversed by JNK inhibition and increased pro-apoptotic caspase-3 expression. In young experimental rats, SIRT1 activation decreased the phosphorylation of stress-induced JNK, ERK, caspase-3, and increased the phosphorylation of AKT after CI. Inhibition of SIRT1 reversed the protective effect of resveratrol. More importantly, in human patients, SIRT1 expression, phosphorylation of JNK/ERK/MAPK/AKT signaling and caspase-3 were up-regulated. In conclusion, SIRT1 could possibly be involved in the modulation of JNK/ERK/MAPK/AKT signaling pathway in experimental rats and humans after CI.

Vitamin E: protective role of a Janus molecule

2001 ◽  
Vol 15 (13) ◽  
pp. 2314-2325 ◽  
Author(s):  
ROBERTA RICCIARELLI ◽  
JEAN-MARC ZINGG ◽  
ANGELO AZZI
Keyword(s):  
Vitamin E ◽  
Protective Role

Association between alcohol-induced oxidative stress and membrane properties in synaptosomes: A protective role of vitamin E

2017 ◽  
Vol 63 ◽  
pp. 60-65 ◽  
Author(s):  
Vaddi Damodara Reddy ◽  
Pannuru Padmavathi ◽  
Saradamma Bulle ◽  
Ananda Vardhan Hebbani ◽  
Shakeela Begum Marthadu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Protective Role ◽  
Membrane Properties

scholarly journals The expression and role of β3AR protein in myocardial ischemia/reperfusion in rats

2021 ◽  
Author(s):  
Zi-Long Wang ◽  
Xiao-Chen Sun ◽  
Rong Luo ◽  
Dong-Ye Li ◽  
Hao-Chen Xuan
Keyword(s):  
Myocardial Ischemia ◽  
Protein Expression ◽  
Caspase 3 ◽  
Sham Group ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Sd Rats ◽  
Group I ◽  
Myocardial Ischemia Reperfusion

IntroductionTo explore serum norepinephrine (NE) concentration and β3-adrenoceptor (β3AR) protein expression at different times during myocardial ischemia/reperfusion (I/R) and examine the role of β3AR in I/R.Material and methods28 Sprague-Dawley (SD) rats were randomly divided into one sham group and six I/R groups. The rats in the I/R groups were subjected to ischemia for 45 minutes. After reperfusion, the serum NE concentration and the β3AR protein expression in the myocardial tissue of the left ventricular injury region were detected. Another 18 SD rats were randomly divided into a sham group, I/R groups, and I/R + BRL37344 group.ResultsCompared with the sham group, the serum NE concentration of rats in the I/R groups significantly increased at 6 hours (P < 0.001). The serum NE concentration and myocardial β3AR protein expression were both highest at 72 hours. Compared with the sham group, the expressions of the pro-apoptotic proteins Bax and cleaved caspase-3 after I/R were significantly increased (P < 0.01, P < 0.001, respectively), and the expression of anti-apoptotic protein Bcl-2 was significantly decreased (P < 0.01). Compared with I/R groups, the expressions of Bax and cleaved caspase-3 in the I/R + BRL37344 group were significantly decreased (P < 0.05, P < 0.01, respectively).ConclusionsWith the prolongation of myocardial I/R in rats, serum NE concentration and β3AR protein expression showed a significant increase trend and reached a peak at 72 hours. Specific β3AR agonist BRL37344 can reduce myocardial I/R injury in vivo in rats, alleviate apoptosis, reduce infarct size, and improve cardiac function.

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