scholarly journals Translocator Protein Modulation by 4′-Chlorodiazepam and NO Synthase Inhibition Affect Cardiac Oxidative Stress, Cardiometabolic and Inflammatory Markers in Isoprenaline-Induced Rat Myocardial Infarction

2021 ◽  
Vol 22 (6) ◽  
pp. 2867
Author(s):  
Ana Ilic ◽  
Dusan Todorovic ◽  
Slavica Mutavdzin ◽  
Novica Boricic ◽  
Biljana Bozic Nedeljkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Cardiac Tissue ◽  
Troponin T ◽  
Serum Levels ◽  
Translocator Protein ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

The possible cardioprotective effects of translocator protein (TSPO) modulation with its ligand 4′-Chlorodiazepam (4′-ClDzp) in isoprenaline (ISO)-induced rat myocardial infarction (MI) were evaluated, alone or in the presence of L-NAME. Wistar albino male rats (b.w. 200–250 g, age 6–8 weeks) were divided into 4 groups (10 per group, total number N = 40), and certain substances were applied: 1. ISO 85 mg/kg b.w. (twice), 2. ISO 85 mg/kg b.w. (twice) + L-NAME 50 mg/kg b.w., 3. ISO 85 mg/kg b.w. (twice) + 4′-ClDzp 0.5 mg/kg b.w., 4. ISO 85 mg/kg b.w. (twice) + 4′-ClDzp 0.5 mg/kg b.w. + L-NAME 50 mg/kg b.w. Blood and cardiac tissue were sampled for myocardial injury and other biochemical markers, cardiac oxidative stress, and for histopathological evaluation. The reduction of serum levels of high-sensitive cardiac troponin T hs cTnT and tumor necrosis factor alpha (TNF-α), then significantly decreased levels of serum homocysteine Hcy, urea, and creatinine, and decreased levels of myocardial injury enzymes activities superoxide dismutase (SOD) and glutathione peroxidase (GPx) as well as lower grades of cardiac ischemic changes were demonstrated in ISO-induced MI treated with 4′-ClDzp. It has been detected that co-treatment with 4′-ClDzp + L-NAME changed the number of registered parameters in comparison to 4′-ClDzp group, indicating that NO (nitric oxide) should be important in the effects of 4′-ClDzp.

scholarly journals Potential Protective Effect of Vitamin C on Qunalphos-Induced Cardiac Toxicity: Histological and Tissue Biomarker Assay

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 39
Author(s):  
Ayed A. Shati ◽  
Mohamed Samir A. Zaki ◽  
Youssef A. Alqahtani ◽  
Mohamed A. Haidara ◽  
Mubarak Al-Shraim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Protective Effect ◽  
Cardiac Tissue ◽  
Electron Microscopic Examination ◽  
Male Rats ◽  
Cardiac Damage ◽  
Electron Microscopic ◽  
Necrosis Factor Alpha ◽  
Vit C

Insecticides and toxicants abound in nature, posing a health risk to humans. Concurrent exposure to many environmental contaminants has been demonstrated to harm myocardial performance and reduce cardiac oxidative stress. The purpose of this research was to study the protective effect of vitamin C (Vit C) on quinalphos (QP)-induced cardiac tissue damage in rats. Eighteen albino male rats were randomly categorised into three groups (n = 6). Control, QP group: rats received distilled water. QP insecticide treatment: an oral administration of QP incorporated in drinking water. QP + Vit C group: rats received QP and Vit C. All the experiments were conducted for ten days. Decline of cardiac antioxidant biomarkers catalase (CAT) and reduced glutathione (GPx) along with increased proinflammatory markers tumour necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) indicated oxidative and inflammatory damage to the heart following administration of QP when compared to control rats. The light microscopic and ultrastructure appearance of QP-treated cardiomyocytes exhibited cardiac damage. Administration of Vit C showed decreased oxidative and inflammatory biomarkers, confirmed with histological and electron microscopic examination. In conclusion, Vit C protected the heart from QP-induced cardiac damage due to decreased inflammation and oxidative stress.

scholarly journals Anti-Inflammatory and Antioxidative Effects of Sumatriptan Against Doxorubicin-Induced Cardiotoxicity in Rat

2021 ◽  
Author(s):  
Mohammad Sheibani ◽  
Hedyeh Faghir-Ghanesefat ◽  
Yaser Azizi ◽  
Tahmineh Mokhtari ◽  
Hasan Yousefi‐Manesh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Mortality Rate ◽  
Cardiac Tissue ◽  
The Body ◽  
Male Rats ◽  
Protective Effects ◽  
Cardiac Damage ◽  
Necrosis Factor Alpha ◽  
Antioxidative Effects

The clinical use of doxorubicin as a potent chemotherapeutic agent is limited due to its dose-dependent cardiotoxicity. Oxidative stress and inflammatory pathways have a pivotal role in doxorubicin-induced cardiotoxicity. Sumatriptan, a 5-hydroxytryptamine (5-HT)1B/1D agonist that is mainly used to relieve migraine pain, has suggested exerting protective effects in numerous pathological conditions through antiinflammatory properties. The aim of the present study was to investigate the effects of sumatriptan on doxorubicin-induced cardiotoxicity and the contribution of anti-inflammation and antioxidative responses. Cardiotoxicity was induced by the administration of doxorubicin three times a week (2.5 mg/kg i.p) for two consecutive weeks on male rats. The animals were divided into four groups, including Control, Sumatriptan (0.1 mg/kg) received group, doxorubicin received group, and Doxorubicin+Sumatriptan (0.1 mg/kg) received group. Sumatriptan was administered 30 min before every injection of doxorubicin. On the last day of the second week, the body weight, mortality rate, electrocardiogram (ECG) and histopathological changes, cardiac inotropic study, and biochemical factors were evaluated. The loss of body weight, mortality rate, ECG parameters, reduction of papillary muscle contractility force as well as histopathological scores following administration of doxorubicin indicated severe cardiac damage. However, treatment with sumatriptan inhibited the functional and structural impairment induced by doxorubicin. In addition, sumatriptan could significantly reduce cardiac tissue levels of malondialdehyde (MDA) and tumor necrosis factor-alpha (TNF-α), which were increased in the doxorubicin-treated rats. This study illustrated the protective effects of sumatriptan on decreasing doxorubicin-induced cardiac toxicity and mortality rate in part through inhibition of inflammatory and oxidative stress pathways.

scholarly journals Melatonin Alleviated Potassium Dichromate-Induced Oxidative Stress and Reprotoxicity in Male Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Samir A. E. Bashandy ◽  
Hossam Ebaid ◽  
Jameel Al-Tamimi ◽  
Omar A.-H. Ahmed-Farid ◽  
Enayat A. Omara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Sperm Count ◽  
Potassium Dichromate ◽  
Reproductive Toxicity ◽  
Male Rats ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Melatonin Administration ◽  
Factor Alpha

Melatonin (ML) is a potent antioxidant that reduces oxidative stress. This study was designed to examine the protective effect of melatonin on potassium dichromate- (PDC-) induced male reproductive toxicity. Forty rats were divided into five groups: the control group, rats administered PDC orally (10 mg/kg body weight) for eight weeks, rats administered ML intraperitoneally at doses of either 2.5 or 5 mg/kg followed by the administration of PDC, and rats administered 5 mg/kg ML only. The treatment of rats with PDC led to a decrease in the levels of plasma sex hormones, glutathione, superoxide dismutase, catalase, carnitine, sperm count, and motility. Testicular malondialdehyde levels, nitric oxide concentrations, and abnormalities increased significantly in the PDC group. Melatonin administration to the PDC-treated rats reduced the increase of malondialdehyde and restored the activity of antioxidant enzymes (superoxide dismutase and catalase), glutathione, and sex hormone levels. Moreover, ML attenuated PDC-induced increase in levels of tumor necrosis factor-alpha or interleukin-6. ML alleviated histopathological changes and an increase of p53-positive immune reaction due to PDC. Furthermore, ML inhibited PDC-induced decrease in the DNA content of spermatogenic cells. This study proposed that melatonin may be useful in mitigating oxidative stress-induced testicular damage due to potassium dichromate toxicity.

scholarly journals Antioxidant Potential ofSpirulina platensisMitigates Oxidative Stress and Reprotoxicity Induced by Sodium Arsenite in Male Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Samir A. E. Bashandy ◽  
Sally A. El Awdan ◽  
Hossam Ebaid ◽  
Ibrahim M. Alhazza
Keyword(s):  
Oxidative Stress ◽  
Sperm Count ◽  
Therapeutic Option ◽  
Testicular Tissue ◽  
Protective Role ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Necrosis Factor Alpha ◽  
Sperm Abnormalities ◽  
Factor Alpha

The present study aimed to examine the protective role ofSpirulina platensis(S. platensis) against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2at a dose of 6.3 mg/kg body weight for 8 weeks) caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD), catalase (CAT), reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH), triiodothyronine (T3), and thyroxine (T4) levels and reduced sperm motility and sperm count. Arsenic (AS) led to a significant increase in testicular malondialdehyde (MDA), tumour necrosis factor alpha (TNF-α), nitric oxide (NO), and sperm abnormalities.S. platensisat a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity.S. platensismay represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication.

Insulin Suppresses Type 1 Diabetes Mellitus-Induced Ventricular Cardiomyocyte Damage Associated with the Inhibition of Biomarkers of Inflammation and Oxidative Stress in Rats

Pharmacology ◽  
2019 ◽  
Vol 104 (3-4) ◽  
pp. 157-165 ◽  
Author(s):  
Mohammad Dallak ◽  
Bahjat Al-Ani ◽  
Dina H. Abdel Kader ◽  
Refaat A. Eid ◽  
Mohamed A. Haidara
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Serum Levels ◽  
Left Ventricular ◽  
Daily Injection ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

Aims: We sought to determine whether insulin can protect against type 1 diabetes mellitus (T1DM)-induced cardiac ultrastructural alterations in an animal model of the disease. This has not been investigated before. Methods: Rats were either injected once with 65 mg/kg streptozotocin (STZ) before being sacrificed after 8 weeks or were treated with a daily injection of insulin 2 days by STZ and continued until being sacrificed. Results: Harvested tissues obtained from left ventricles in the untreated T1DM rats showed substantial damage to the cardiomyocyte ultrastructure as demonstrated by disintegrated myofibrils and their sarcomeres, damaged mitochondria and lipid droplets, which was substantially protected by insulin. Insulin also significantly inhibited T1DM-induced hyperglycemia (p < 0.001), dyslipidemia (p < 0.0001), malondialdehyde (MDA; p < 0.0001), tumor necrosis factor-alpha (TNF-α; p < 0.001) and interleukin-6 (p < 0.001). We further demonstrated a significant (p ≤ 0.001) correlation between either sarcomere or mitochondrial injury scoring and the serum levels of glucose, dyslipidemia, and biomarkers of oxidative stress (OxS) and inflammation. Conclusions: These results indicate that insulin effectively suppresses left ventricular cardiomyocyte ultrastructural damage, which substantially slows down the progression of diabetic cardiomyopathy for 8 weeks in a rat model of T1DM, possibly due to the glycemic control and inhibition of dyslipidemia, OxS and inflammation.

The ameliorative effect of thymol against hydrocortisone-induced hepatic oxidative stress injury in adult male rats

2015 ◽  
Vol 93 (4) ◽  
pp. 282-289 ◽  
Author(s):  
Hanaa R. Aboelwafa ◽  
Hany N. Yousef
Keyword(s):  
Oxidative Stress ◽  
Adult Male ◽  
Serum Levels ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Stress Injury ◽  
Ultrastructural Alterations ◽  
Oxidative Stress Injury ◽  
Tnf Α ◽  
Ameliorative Effect

The aim of the present study was to investigate whether hydrocortisone induces oxidative stress in hepatocytes and to evaluate the possible ameliorative effect of thymol against such hepatic injury. Twenty-four adult male rats were divided into control, thymol, hydrocortisone, and hydrocortisone+thymol groups. The 4 groups were treated daily for 15 days. Hydrocortisone significantly induced oxidative stress in the liver tissues, marked by increased serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total oxidative capacity (TOC), and tumor necrosis factor-alpha (TNF-α) accompanied by marked decline of serum levels of total protein, albumin, and total antioxidant capacity (TAC). Also, marked elevation in the levels of the thiobarbituric acid reactive substances (TBARS) and TNF-α, beside significant decrease in the level of glutathione (GSH) in hepatic tissues were recorded. These biochemical alterations were accompanied by histopathological changes marked by destruction of the normal hepatic architecture, in addition to ultrastructural alterations represented by degenerative features covering almost all the cytoplasmic organelles of the hepatocytes. Supplementation of hydrocortisone-treated rats with thymol reversed most of the biochemical, histological, and ultrastructural alterations. The results of our study confirm that thymol has strong ameliorative effect against hydrocortisone-induced oxidative stress injury in hepatic tissues.

scholarly journals Increased Serum Levels of Tumor Necrosis Factor-Alpha, Resistin, and Visfatin in the Children with Autism Spectrum Disorders: A Case-Control Study

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad Ali Ghaffari ◽  
Elham Mousavinejad ◽  
Forough Riahi ◽  
Masoumeh Mousavinejad ◽  
Mohammad Reza Afsharmanesh
Keyword(s):  
Autism Spectrum Disorders ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Autism Spectrum ◽  
Necrosis Factor Alpha ◽  
Children With Asd ◽  
Factor Alpha ◽  
Spectrum Disorders ◽  
Necrosis Factor

Background. Autism spectrum disorders (ASDs) are complex disorders where the pathogenesis is not fully understood. Several proinflammatory and immunoinflammatory disturbances have been observed in the etiology of ASD. There is, however, limited knowledge on variations of adipokines in ASD. The present study aimed to analyze the serum levels of resistin, visfatin, and tumor necrosis factor-alpha (TNF-α) in children with ASD in relation to body weight, gender, and ASD severity level. Method. In total, 30 children with ASD (mean age: 7.72±2.65 y; range; 4–12 y) and 30 healthy children (mean age: 8.4±2.66 y; range: 4–12 y), including males and females, were matched for age, gender, and body mass index (BMI). Serum samples were collected, and visfatin, resistin, and TNF-α serum levels were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Result. Serum visfatin, resistin, and TNF-α levels in children with ASD were significantly higher than that in the healthy patients (p<0.05). Two significant correlations were found: a correlation between resistin and visfatin with TNF-α in children with ASD (R = 0.8 and R = 0.62, resp.) and a correlation between resistin and visfatin in children with ASD (R = 0.66). Conclusion. Higher TNF-α, resistin, and visfatin levels were found in children with ASD in comparison with controls, suggesting that elevated levels of serum proinflammatory agents may be implicated in the pathophysiology of ASD.

Leucocyte-depleted cardioplegia does not reduce reperfusion injury in hypothermic coronary artery bypass surgery

Perfusion ◽  
1999 ◽  
Vol 14 (5) ◽  
pp. 371-377 ◽  
Author(s):  
P G Browning ◽  
M Pullan ◽  
M Jackson ◽  
A Rashid
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery ◽  
Coronary Artery Bypass ◽  
Coronary Artery Bypass Surgery ◽  
Myocardial Injury ◽  
Bypass Surgery ◽  
Troponin T ◽  
Artery Bypass ◽  
Oxidized Glutathione ◽  
Patient Groups

This study investigated the effects of leucocyte-depleted cardioplegia on postreperfusion oxidative stress and myocardial injury in elective hypothermic coronary artery bypass surgery. Forty patients were randomized to receive either cardioplegia with leucocytes depleted by an in-line Pall BC1B filter, or blood cardioplegia without leucocyte depletion. Transmyocardial oxidative stress was assessed by oxidized glutathione measurements in samples taken simultaneously from the coronary sinus and aortic root, and myocardial injury by postoperative CKMB and troponin-T measurements. The BC1B filters reduced numbers of cardioplegia leucocytes by a mean of 90.7%. Both patient groups demonstrated significant increases ( p < 0.001) in transcardiac oxidized glutathione gradients after crossclamp release. No significant differences were found between the groups for postreperfusion oxidized glutathione gradients, postoperative levels of CKMB or troponin-T, or in the frequency of perioperative and postoperative complications. These results suggest that leucocyte-depleted cardioplegia does not significantly improve myocardial protection in patients undergoing elective coronary artery bypass surgery.

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