Atorvastatin inhibits brain oxidative stress of Streptozotocininduced diabetic rat

2013 ◽  
Vol 1 (1) ◽  
pp. 35
Author(s):  
Mohammad Taghi Mohammadi ◽  
Mojtaba Gaedniaye Jahromi ◽  
Mohammad Hossein Mirjalili ◽  
Mehdi Ramezani Binabaj ◽  
Mahvash Jafari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Atorvastatin Treatment ◽  
Increase Blood Glucose ◽  
Increase Blood Glucose Level ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

It is well known that production of ROS compounds and generation of oxidative stress during diabetes are the most important mechanisms of tissue damage. The aim of this study was to examine the effects of atorvastatin treatment, as an antioxidant, to prevent the brain tissue oxidative stress in streptozotocin-induced diabetic rats. Male Wistar rats were randomly divided into four groups (five rats in each group) as followed: normal, normal treated was orally received 20 mg/kg/day atorvastatin for 30 days, diabetic group was given 40 mg/kg streptozotocin by intravenous injection and diabetic treated similar to normal treated rats. After 30 days of treatment, rats were sacrificed under deep anesthesia to remove the brain. After tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods. In addition to increase blood glucose level in diabetic rats (78%), brain SOD and CAT activities were significantly increased compared with normal rats. Also, diabetes significantly decreased the GSH content of brain tissue by 57%, and increased the brain MDA level by 35%. Finally treatment with atorvastatin significantly decreased the augmented brain CAT activity and the MDA level during diabetes. Based on the finding of this study, diabetes-induced hyperglycemia provoked the production of free radicals in the brain tissue that leading to oxidative stress. Also, treatment with atorvastatin may have prevented from hyperglycemia-induced oxidative stress in the brain of diabetic rat.

Protocatechuic acid protects brain mitochondrial function in streptozotocin-induced diabetic rats

2015 ◽  
Vol 40 (10) ◽  
pp. 1078-1081 ◽  
Author(s):  
Yoswaris Semaming ◽  
Jirapas Sripetchwandee ◽  
Piangkwan Sa-nguanmoo ◽  
Hiranya Pintana ◽  
Patchareewan Pannangpetch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Glycemic Control ◽  
Mitochondrial Dysfunction ◽  
Stress Reduction ◽  
Mitochondrial Function ◽  
Protocatechuic Acid ◽  
Diabetic Rats ◽  
Brain Oxidative Stress ◽  
The Brain ◽  
Brain Mitochondrial Function

Brain mitochondrial dysfunction has been demonstrated in diabetic animals with neurodegeneration. Protocatechuic acid (PCA), a major metabolite of anthocyanin, has been shown to exert glycemic control and oxidative stress reduction in the heart. However, its effects on oxidative stress and mitochondrial function in the brain under diabetic condition have never been investigated. We found that PCA exerted glycemic control, attenuates brain mitochondrial dysfunction, and contributes to the prevention of brain oxidative stress in diabetic rats.

Anxiety-related behavior in hyperhomocysteinemia induced by methionine nutritional overload in rats: role of the brain oxidative stress

2016 ◽  
Vol 94 (10) ◽  
pp. 1074-1082 ◽  
Author(s):  
Dragan Hrncic ◽  
Jelena Mikić ◽  
Aleksandra Rasic-Markovic ◽  
Milica Velimirović ◽  
Tihomir Stojković ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Open Field ◽  
Wistar Rats ◽  
Brain Regions ◽  
Oxidative Status ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
The Brain

The aim of this study was to examine the effects of a methionine-enriched diet on anxiety-related behavior in rats and to determine the role of the brain oxidative status in these alterations. Adult male Wistar rats were fed from the 30th to 60th postnatal day with standard or methionine-enriched diet (double content comparing with standard diet: 7.7 g/kg). Rats were tested in open field and light–dark tests and afterwards oxidative status in the different brain regions were determined. Hyperhomocysteinemia induced by methionine-enriched diet in this study decreased the number of rearings, as well as the time that these animals spent in the center of the open field, but increased index of thigmotaxy. Oxidative status was selectively altered in the examined regions. Lipid peroxidation was significantly increased in the cortex and nc. caudatus of rats developing hyperhomocysteinemia, but unaltered in the hippocampus and thalamus. Based on the results of this research, it could be concluded that hyperhomocysteinemia induced by methionine nutritional overload increased anxiety-related behavior in rats. These proanxiogenic effects could be, at least in part, a consequence of oxidative stress in the rat brain.

scholarly journals Protective Effects of Beta Glucan and Gliclazide on Brain Tissue and Sciatic Nerve of Diabetic Rats Induced by Streptozosin

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Harun Alp ◽  
Sefer Varol ◽  
Muhammet Murat Celik ◽  
Murat Altas ◽  
Osman Evliyaoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sciatic Nerve ◽  
Neuroprotective Effect ◽  
Diabetic Rats ◽  
Nerve Tissue ◽  
Stress Index ◽  
Diabetic Rat ◽  
Beta Glucan ◽  
The Brain ◽  
Antioxidant Effects

There have not been yet enough studies about effects of beta glucan and gliclazide on oxidative stress created by streptozotocin in the brain and sciatic nerve of diabetic rats. The aim of this paper was to investigate the antioxidant effects of gliclazide and beta glucan on oxidative stress and lipid peroxidation created by streptozotosin in brain and sciatic nerve. Total of 42 rats were divided into 6 groups including control, diabetic untreated (DM) (only STZ, diabetic), STZ (DM) + beta glucan, STZ (DM) + gliclazide, only beta glucan treated (no diabetic), and only gliclazide treated (no diabetic). The brain and sciatic nerve tissue samples were analyzed for malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and paraoxonase (PON-1) levels. We found a significant increase in MDA, TOS, and OSI along with a reduction in TAS level, catalase, and PON-1 activities in brain and sciatic nerve of streptozotocin-induced diabetic rats. Also, this study shows that in terms of these parameters both gliclazide and beta glucan have a neuroprotective effect on the brain and sciatic nerve of the streptozotocin-induced diabetic rat. Our conclusion was that gliclazide and beta glucan have antioxidant effects on the brain and sciatic nerve of the streptozotocin-induced diabetic rat.

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

Effect of atorvastatin on the angiogenic responsiveness of coronary endothelial cells in normal and streptozotocin (STZ) induced diabetic rats

2014 ◽  
Vol 92 (4) ◽  
pp. 338-349 ◽  
Author(s):  
Kiranj K. Chaudagar ◽  
Anita A. Mehta
Keyword(s):  
Endothelial Cells ◽  
Low Dose ◽  
Ischemia Reperfusion ◽  
Late Phase ◽  
Diabetic Rats ◽  
Lipid Lowering ◽  
Diabetic Rat ◽  
High Dose ◽  
Atorvastatin Treatment ◽  
Coronary Endothelial Cells

Atorvastatin, a lipid lowering agent, possesses various pleiotropic vasculoprotective effects, but its role in coronary angiogenesis is still controversial. Our objective was to study the effects of atorvastatin on the angiogenic responsiveness of coronary endothelial cells (cEC) from normal and diabetic rats. Male Wistar rats were distributed among 9 groups; (i) normal rats, (ii) 30 day diabetic rats, (iii) 60 day diabetic rats, (iv) normal rats administered a low dose of atorvastatin (1 mg/kg body mass, per oral (p.o.), for 15 days); (v) 30 day diabetic rats administered a low dose of atorvastatin; (vi) 60 day diabetic rats administered a low dose of atorvastatin; (vii) normal rats administered a high dose of atorvastatin (5 mg/kg, p.o., for 15 days); (viii) 30 day diabetic rats administered a high dose of atorvastatin; (ix) 60 day diabetic rats administered a high dose of atorvastatin. Each group was further divided into 2 subgroups, (i) sham ischemia–reperfusion and (ii) rats hearts that underwent ischemia–reperfusion. Angiogenic responsiveness the and nitric oxide (NO) releasing properties of the subgroups of cECs were studied using a chorioallantoic membrane assay and the Griess method, respectively. Atorvastatin treatment significantly increased VEGF-induced angiogenic responsiveness and the NO-releasing properties of cECs from all of the subgroups, compared with their respective non-treated subgroups except for the late-phase diabetic rat hearts that underwent ischemia–reperfusion, and the high dose of atorvastatin treatment groups. These effects of atorvastatin were significantly inhibited by pretreatment of cECs with l-NAME, wortmannin, and chelerythrine. Thus, treatment with a low dose of atorvastatin improves the angiogenic responsiveness of the cECs from normal and diabetic rats, in the presence of VEGF, via activation of eNOS–NO release.

scholarly journals Effects of Apocynin on Heart Muscle Oxidative Stress of Rats with Experimental Diabetes: Implications for Mitochondria

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 335
Author(s):  
Estefanía Bravo-Sánchez ◽  
Donovan Peña-Montes ◽  
Sarai Sánchez-Duarte ◽  
Alfredo Saavedra-Molina ◽  
Elizabeth Sánchez-Duarte ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Sensitivity ◽  
Cardiac Tissue ◽  
Diabetic Rats ◽  
Oxidase Inhibitor ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Transport Chain ◽  
Male Wistar Rats

Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the β-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

Dietary Choline Deprivation Exacerbates Cardiomyopathy in Streptozotocin-Induced Diabetic Adult Rats

Diabetology ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 190-204
Author(s):  
Ahmed Al-Humadi ◽  
Athina Strilakou ◽  
Hussam Al-Humadi ◽  
Rafal Al-Saigh ◽  
Emmanouel Agapitos ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Dietary Intervention ◽  
Myocardial Dysfunction ◽  
Posterior Wall ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Myocardial Inflammation ◽  
Standard Diet ◽  
Adult Rats ◽  
Male Wistar Rats

Choline (Ch) is an essential molecule of substantial importance for the optimal development and function of several biological systems. Ch deprivation has been linked with abnormal fat metabolism, insulin resistance, and myocardial dysfunction. The current study provides evidence of an exacerbation of streptozotocin-induced cardiomyopathy in adult diabetic Wistar rats by dietary Ch deprivation through the administration of a Ch-deprived diet (CDD). Twenty-four adult male Wistar rats were randomly separated into four groups: control, diabetic (DM), choline-deprived through choline-deprived diet (CD), and diabetic choline-deprived (DM + CD). After five weeks of dietary intervention, myocardium echocardiographic and histological assessments were performed. Choline-deprived diabetic rats exhibited significantly slower heart rate, significantly higher myocardial ejection velocity and left ventricle wall tension index with a concomitant significant decreased LV posterior wall thickness as compared to diabetic rats fed on a standard diet. Moreover, histopathological evidence demonstrated an exacerbation of myocardial inflammation and fibrosis associated with significant up-regulation of VEGF expression in the diabetic rat myocardium as a result of Ch deprivation. The study’s findings are of particular significance since the examined experimental approach introduces a previously uncharacterised comorbidity simulation with regards to myocardial structure and functional profiling.

scholarly journals Ellagic Acid ameliorates Streptozotocin-Induced Diabetic Hyperalgesia in Rat: Involvement of Oxidative Stress

2021 ◽  
Author(s):  
Siamak Shahidi ◽  
◽  
Alireza Komaki ◽  
Safoura Raoufi ◽  
Iraj Salehi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ellagic Acid ◽  
Therapeutic Potential ◽  
Biological Activities ◽  
Antinociceptive Effect ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Tail Flick ◽  
Stress Markers ◽  
Total Antioxidant

Background/Aim: Hyperalgesia is one of the current complications of diabetes mellitus that Oxidative stress and inflammation have principal role in its development. Ellagic Acid (EA) as a herbal component, has some biological activities, including antioxidant and anti-inflammatory effects. This study was designed to evaluate the possible beneficial effect of EA on hyperalgesia in streptozotocin (STZ)-induced diabetic rat. Materials and Methods: Rats were divided into control(vehicle received), diabetic, EA (25, 50 mg/kg)-treated control and EA(25, 50 mg/kg)-treated diabetic groups. Diabetes was induced by a single intraperitoneal (IP) injection of streptozotocin (STZ) (60 mg/Kg). EA was administered daily by oral gavage for 4 weeks. Hyperalgesia was assessed using tail flick (TF) and hot plate (HP) tests. Also, oxidative stress markers including malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC) in the serum were evaluated. Results: Diabetic animals showed marked reductions in TF and HP latencies, elevation of serum MDA level and TOS and diminution of serum TAC compared to controls significantly. Treatment of Diabetic rats with EA ameliorated reduction of TF latency at the dose of 25 mg/kg and HP latency at the dose of 50 mg/kg. Furthermore EA significantly increased TAC and decreased MDA level at dose of 50 mg/kg and reduced TOS at both doses in the serum of diabetic animals. In EA treated normal rats we could see no significant alterations in the parameters studied. Conclusion: These results displayed potent antinociceptive effect of EA in diabetic rats via attenuating oxidative stress. This proposes therapeutic potential of EA for damping diabetic hyperalgesia.

scholarly journals Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiac Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Serum Adiponectin ◽  
Diabetic Rat ◽  
Lv Function ◽  
High Dose ◽  
And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

Sign in / Sign up

Export Citation Format

Share Document