scholarly journals Chitosan and Curcumin Nanoformulations against Potential Cardiac Risks Associated with Hydroxyapatite Nanoparticles in Wistar Male Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Israa F. Mosa ◽  
Haitham H. Abd ◽  
Abdelsalam Abuzreda ◽  
Amenh B. Yousif ◽  
Nadhom Assaf
Keyword(s):  
Cardiac Tissue ◽  
Chitosan Nanoparticles ◽  
Mitochondrial Pathway ◽  
Serum Markers ◽  
Male Rats ◽  
Circulation System ◽  
Hydroxyapatite Nanoparticles ◽  
Necrosis Factor Alpha ◽  
Curcumin Nanoparticles ◽  
Blood Circulation System

Nanoparticle-induced cardiovascular diseases have attracted much attention. Upon entering the blood circulation system, these particles have the potency to induce cardiomyocytes, leading to cardiac failure or myocardial ischemia, and the molecular mechanism remains to be completely clarified. In this study, the cardiac toxicity of rats orally exposed to hydroxyapatite nanoparticles (HAPNPs) has been observed through an increase in myocardial infarction serum markers including CK-MB and alterations in routine blood factors, expression of apoptosis-related protein P53, and increased levels of serum inflammatory markers represented by the tumor necrosis factor alpha and Interleukin-6, as well as a decline in heart antioxidant enzymes and reduced glutathione level, while an induction in lipid peroxidation and nitric oxide has been observed, as well as notable histological and histochemical alterations in the heart of these animals. mRNA and protein expressions of vascular endothelial growth factor (VEGF-A), cyclooxygenase-2 (COX-2), and atrial natriuretic factor (ANF) were elevated in the myocardium. However, the coadministration of chitosan nanoparticles (CsNPs) and/or curcumin nanoparticles (CurNPs) successfully modulated these alterations and induced activation in antioxidant parameters. The present data suggest that HAPNPs-induced apoptosis via the mitochondrial pathway may play a crucial role in cardiac tissue damage and the early treatment with CsNPs and CurNPs may protect the heart from infarction induced by HAPNPs toxic effect.

scholarly journals Synergistic antioxidant capacity of CsNPs and CurNPs against cytotoxicity, genotoxicity and pro-inflammatory mediators induced by hydroxyapatite nanoparticles in male rats

2019 ◽  
Vol 8 (6) ◽  
pp. 939-952 ◽  
Author(s):  
Israa F. Mosa ◽  
Mokhtar Youssef ◽  
Maher Kamel ◽  
Osama F. Mosa ◽  
Yasser Helmy
Keyword(s):  
Gene Expression ◽  
Biochemical Parameters ◽  
Chitosan Nanoparticles ◽  
Kidney Injury ◽  
Toxicity Assessment ◽  
Male Rats ◽  
Lipocalin 2 ◽  
Hydroxyapatite Nanoparticles ◽  
Curcumin Nanoparticles ◽  
Kidney Injury Molecule 1

Abstract Due to their dynamic characteristics, hydroxyapatite nanoparticles (HAP-NPs) have been employed numerous times in nanomedicine and in tissue engineering, particularly as diagnostic and therapeutic agents. However, there are outstanding findings from various studies that question whether these NPs are safe when they are used in the human body. Therefore, a more in-depth toxicity assessment should be carried out to give a clear answer regarding the fate of these particles. Here we aim to investigate the possible cytotoxicity, genotoxicity and inflammation induced by HAP-NPs, as well as predict the synergistic antioxidative effect of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in mitigating this pronounced toxicity. The present study was conducted on eighty Wistar male rats, divided into eight equal groups. The results showed that, at the molecular level, HAP-NPs significantly induced gene expression of tumor suppressor protein p53, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and also Kidney Injury Molecule-1 (KIM-1) and Lipocalin-2 (LCN2). In addition, kidney biochemical parameters (total bilirubin, urea, uric acid and creatinine) increased, but albumin levels decreased in the group treated with HAP-NPs alone. Meanwhile, co-treatment with CsNPs and/or CurNPs with HAP-NPs showed an improvement in the activities of the kidney parameters and reduced inflammation. This study shows that the nephrotoxicity mechanism of HAP-NPs may involve various signaling pathways including alterations in biochemical parameters, gene expression of KIM-1 and LCN2 and disturbing the production of cytokines and p53. Furthermore, these insights showed that the combined effect of both CsNPs and CurNPs was more pronounced than the effect of each one on its own.

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 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.

STUDY OF THE PREVALENCE OF DENTOALVEOLAR ANOMALIES, INCLUDING DISTAL BITE IN CHILDREN AND ADOLESCENTS

Vestnik ◽  
2021 ◽  
pp. 133-137
Author(s):  
Г.Т. Ермуханова ◽  
А.О. Етекбаева
Keyword(s):  
Children And Adolescents ◽  
Blood Circulation ◽  
Circulation System ◽  
Dental Anomalies ◽  
Functional Changes ◽  
Facial Region ◽  
Blood Circulation System ◽  
Lateral Segment ◽  
Distal Occlusion ◽  
Maxillary Region

В данной статье описывается изучение распространенности зубочелюстных аномалий, в том числе и дистального прикуса среди детей и подростков школьного возраста. В настоящее время широко распространены зубочелюстные аномалии, в том числе дистальный прикус среди детей и подростков. Зубочелюстные аномалии приводят к функциональной патологии морфологических нарушений челюстной области. Изменения возрастно увеличиваются и сопровождаются деформацией лицевой области черепа наряду с эстетическими отклонениями.У больных часто наблюдаются нарушения положения позвоночника,функциональные изменения в системе малого кровообращения и задержка психосомтического развития.Это говорит о ранних нарушениях профилактики и несвоевременном оказании ортодонтической,зубопротезной и комплексной медицинской помощи.В связи с этим важную роль играет эпидемиологическая ситуация по зубной аномалии. исполняют информацию. Диагноз дистальной окклюзии называется боковым сегментом верхнего зубного ряда, расположенным перед боковым сегментом нижнего зубного ряда и появлением между ними дистальной стадии. Лечение и прогноз дистальной окклюзии зубного ряда зависит от возраста больного и характера аномалии [1] The article is devoted to the study of the prevalence of dentition anomalies, including distal occlusion among children and adolescents of school age. Currently, dental anomalies, including distal bite, are widespread among children and adolescents. Dental anomalies lead to functional pathology of morphological disorders of the maxillary region. The changes increase with age and are accompanied by deformation of the facial region of the skull along with aesthetic deviations. Patients often have disorders of the spine position, functional changes in the small blood circulation system and delayed psychosomal development.It tells about the early breaches of the prevention of and untimely provision of orthodontic, prosthodontic and comprehensive medical care.In this regard, an important role is played by the epidemiological situation of dental anomalies. execute information. The diagnosis of distal occlusion is called the lateral segment of the upper dentition, located in front of the lateral segment of the lower dentition and the appearance of the distal stage between them. Treatment and prognosis of distal occlusion of the dentition depends on the patient's age and the nature of the anomalies [1].

Abstract 267: Activation of a Novel Estrogen Receptor Ameliorates Experimental Pulmonary Hypertension in Male Rats

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Gisele Zapata-Sudo ◽  
Allan K Alencar ◽  
Guilherme C Montes ◽  
Sabrina T Martinez ◽  
Aline G Fraga ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Vascular Remodeling ◽  
Systolic Pressure ◽  
New Drugs ◽  
Male Rats ◽  
Exercise Intolerance ◽  
Vehicle Group ◽  
Time To Exhaustion ◽  
Necrosis Factor Alpha ◽  
Pulmonary Vascular Remodeling

Introduction: Pulmonary arterial hypertension (PAH) is characterized by pulmonary vascular remodeling that leads to uncompensated RV failure, and premature death. Preclinical studies have demonstrated that activation of the G protein-coupled estrogen receptor (GPER) is cardioprotective in male rats, and that a selective agonist G1, elicits vascular relaxation in rats of either sex. This work investigated the effects of G1 in male rats with monocrotaline (MCT)-induced PAH. Methods and Results: Male Wistar rats received a single intraperitoneal injection of MCT (60 mg/kg) for PAH induction. Experimental groups were: control, MCT + vehicle, and MCT + G1 (400 μg/kg/day s.c.). Animals were treated with vehicle or G1 for 14 days after the onset of disease (n = 5 per group). Treadmill test and transthoracic echocardiography were performed to access exercise capacity and cardiac function, respectively. RV systolic pressure (RVSP) and mean arterial pressure (MAP) were measured. Time to exhaustion in the treadmill (s) was reduced from 1042.0 ± 66.4 to 188.0 ± 53.1 (MCT + vehicle) and recovered to 809.4 ± 61.5 after G1 treatment. Pulmonary acceleration time (PAT) (ms) was reduced from 44.7 ± 1.4 to 24.7 ± 1.2 in MCT + vehicle group and restored to 41.8 ± 1.0 in MCT + G1 group. RVSP (mmHg) was increased from 24.6 ± 0.6 to 41.1 ± 1.4 (MCT + vehicle) and was reduced to 27.5 ± 0.7 (MCT + G1). MAP (mmHg) was reduced from 100.9 ± 1.1 to 77.1 ± 2.4 (MCT + vehicle), indicating HF induced by the RV dysfunction, and G1 normalized it to 92.4 ± 1.4. G1 decreased pulmonary vascular remodeling and normalized endothelial nitric oxide enzyme levels in lungs from PAH rats. PLB/SERCA2a ratio increased, as a sign of contractility dysfunction, in PAH rats and tumor necrosis factor alpha upregulation was significantly correlated with these Ca 2+ handling proteins impairment. Activation of GPER beneficially reduced PLB/SERCA2a ratio and TNF-α levels in RV tissue of MCT-induced PAH rats. Conclusions: G1 was effective to reverse PAH-induced RV dysfunction and exercise intolerance in male rats, a finding that may have important implications for ongoing clinical evaluation of new drugs for the treatment of the disease.

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