scholarly journals Protective Effect of Hydroalcoholic Extract of Solanum surattense on Brain Tissue Damage and Oxidative Stress in Adult Rats with Toxoplasmosis

2020 ◽  
Vol 1 (1) ◽  
pp. 14-17
Author(s):  
Mansour Ataei ◽  
Arash Khaki ◽  
Yagoob Garedaghi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Female Rats ◽  
Adult Rats ◽  
Hydroalcoholic Extract ◽  
Solanum Surattense ◽  
Brain Tissue Damage ◽  
The Brain

Introduction: Toxoplasmosis is caused by a protozoan named Toxoplasma gondii. This protozoan is a parasite of cats that can spread among other animals and birds around the world and cause a disease that varies from mild to severe. The disease is seen in the forms of acquired toxoplasmosis and congenital toxoplasmosis. Many studies have shown that there is a relationship between reproductive function and toxoplasmosis. T. gondii has led to decreased reproductive performance of males and females in many experimental animals. The aim of this study was to investigate the protective effect of hydroalcoholic extract of Solanum surattense on the brain tissue damage and brain oxidative stress induced by T. gondii in adult rats. Methods: For this purpose, 32 adult female rats were randomly divided into 4 groups. In group 1, 8 healthy rats received IP saline for 3 weeks. In group 2, 8 rats with T. gondii received IP saline for 3 weeks. In group 3, 8 rats with T. gondii received the hydroalcoholic extract of S. surattense for 3 weeks. In group 4, 8 healthy rats received the hydroalcoholic extract of S. surattense for 3 weeks. Then, brain tissue resection was performed to evaluate histological damage and levels of antioxidant enzymes. Results: Histological and biochemical studies showed that T. gondii had a deleterious effect on the brain tissue of rats and increased the level of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). The administration of hydroalcoholic extract of S. surattense improved these effects due to its high antioxidant properties. Conclusion: The administration of the appropriate dose of hydroalcoholic extract of S. surattense for three consecutive weeks had a protective effect on brain tissue exposed to T. gondii.

scholarly journals Acetaldehyde Induces Cytotoxicity of SH-SY5Y Cells via Inhibition of Akt Activation and Induction of Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Tingting Yan ◽  
Yan Zhao ◽  
Xia Zhang
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
Cognitive Dysfunction ◽  
Tissue Damage ◽  
Heavy Drinking ◽  
Mitogen Activated Protein Kinase ◽  
Toxic Metabolite ◽  
Excessive Alcohol Consumption ◽  
Brain Tissue Damage ◽  
Induced Apoptosis

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. It has been shown that heavy drinking is associated with an earlier onset of neurodegenerative diseases such as Alzheimer’s disease. Acetaldehyde, the most toxic metabolite of ethanol, is speculated to mediate the brain tissue damage and cognitive dysfunction induced by the chronic excessive consumption of alcohol. However, the exact mechanisms by which acetaldehyde induces neurotoxicity are not totally understood. In this study, we investigated the cytotoxic effects of acetaldehyde in SH-SY5Y cells and found that acetaldehyde induced apoptosis of SH-SY5Y cells by downregulating the expression of antiapoptoticBcl-2andBcl-xLand upregulating the expression of proapoptoticBax. Acetaldehyde treatment led to a significant decrease in the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). In addition, acetaldehyde induced the activation of p38 mitogen-activated protein kinase (MAPK) while inhibiting the activation of extracellular signal-regulated kinases (ERKs, p44/p42MAPK). Meanwhile, acetaldehyde treatment caused an increase in the production of reactive oxygen species and elevated the oxidative stress in SH-SY5Y cells. Therefore, acetaldehyde induces cytotoxicity of SH-SY5Y cells via promotion of apoptotic signaling, inhibition of cell survival pathway, and induction of oxidative stress.

scholarly journals The Effect of Gender on Brain Tissue Changes Induced by Renal Ischemia-Reperfusion Injury in Adult Rats

2019 ◽  
Vol 8 (2) ◽  
pp. 113-118
Author(s):  
Fakhri Armin ◽  
Fariba Azarkish ◽  
Ali Atash Ab Parvar ◽  
Aghdas Dehghani
Keyword(s):  
Brain Tissue ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Left Kidney ◽  
Renal Ischemia ◽  
Female Rats ◽  
Male Rats ◽  
Adult Rats ◽  
Sensitive Organ ◽  
The Brain

Background: Renal ischemia-reperfusion (RIR) is a common clinical injury that affects the function of other remote organs such as the brain by initiating a cascade of complex and wide-ranging inflammatory responses. RIR also follows a different course in men and women. Since there is little information on the effect of RIR on the brain as a sensitive organ in both males and females, the present research was performed to investigate the effect of gender on RIR-induced brain tissue alterations in adult rats. Materials and Methods: In this study, 28 Wistar rats (14 female and 14 male rats) weighing 200 ± 20 g were divided into the following groups: 1- male sham (MS), 2- female sham (FS), 3- male ischemia (MI) with 3-hour reperfusion (ISC3hr), and 4- Female ischemia (FI) with 3-hour reperfusion (ISC3hr). Bilateral renal ischemia was induced for 45 minutes and blood samples were taken after reperfusion for the measurements of serum blood urea nitrogen (BUN), creatinine (Cr), malondialdehyde (MDA), and nitrite levels. The left kidney was removed for evaluation of MDA and tissue nitrite levels. Right kidney and brain tissue underwent histological examination. Results: Serum BUN level increased in both genders. Serum nitrite level was significantly different between both genders, meaning that it was increased in the female rats as compared to male ones. Overall brain tissue damage was significantly increased in males compared to females. Conclusion: RIR has an effect on the function and tissue of kidney and brain in both genders. Female rats are more susceptible to the nitric oxide system than the male ones. This study showed that male brain tissue was more susceptible to RIR. Therefore, gender is one of the important factors that should be considered in clinical treatments.

scholarly journals Protective Effect of Hydroalcoholic Extract of Orange Peel on PCNA and FSH-R Gene Expression in Histological Damage and Oxidative Stress Due to Ovarian Torsion in Adult Rats

2021 ◽  
Vol 9 (3) ◽  
pp. 205-211
Author(s):  
Seyedeh-Roza Tafrishi Nejad ◽  
Arash Khaki ◽  
Shamci Abbasalizadeh ◽  
Majid Shokoohi ◽  
Nava Ainehchi
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Protective Effect ◽  
Ovarian Tissue ◽  
Orange Peel ◽  
Ovarian Torsion ◽  
R Gene ◽  
Adult Rats ◽  
Hydroalcoholic Extract ◽  
Histological Damage

Objectives: The aim of this study was to evaluate the protective effect of the hydroalcoholic extract of orange peel on proliferating cell nuclear antigen (PCNA) and follicle-stimulating hormone receptor (FSH-R) gene expression in histological injuries and acid stress caused by ovarian torsion in adult rats. Materials and Methods: In this experimental study, 32 adult female rats were randomly divided into 4 groups. In group 1 (Sham), the abdominal wall was cut without applying torsion and in group 2, ovarian torsion was performed for 2 hours, followed by detorsion for 2 weeks. The hydro-alcoholic extract of orange peel was added to their diet for two weeks in group 3, followed by ovarian torsion for 2 hours and detorsion for 2 hours. Group 4 received the orange peel extract for two weeks and after then ovarian resection for the evaluation of histological damage and blood sampling to examine the serum level of antioxidant enzymes, as well as the expression of PCNA and FSH-R genes in the ovarian tissue. Results: Histological changes in the ovary tissue of rats showed that torsion and detorsion have destructive effects on the ovarian tissue, and torsion/detorsion led to a reduction in the expression of PCNA and FSH-R (P < 0.05). Based on biochemical and hormonal results, the ovarian torsion resulted in an imbalance in the oxidative stress markers and hormone profile of rats. Finally, the administration of the hydroalcoholic extract of orange peel due to its high antioxidant properties improves these effects. Conclusions: In general, administering an appropriate dose of the hydroalcoholic extract of orange peel for two consecutive weeks in the diet had a protective effect on the ovarian tissue at the risk of torsion/detorsion.

The beneficial effects of l-cysteine on brain antioxidants of rats affected by sodium valproate

2017 ◽  
Vol 36 (11) ◽  
pp. 1212-1221 ◽  
Author(s):  
RZ Hamza ◽  
NS El-Shenawy
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Protective Effect ◽  
Brain Tissue ◽  
Sodium Valproate ◽  
Histopathological Examination ◽  
Control Group ◽  
High Dose ◽  
Beneficial Effects ◽  
The Brain

Oxidative stress caused by sodium valproate (SV) is known to play a key role in the pathogenesis of brain tissue. The present study was designed to evaluate the protective effect of l-cysteine (LC) on the antioxidants of brain tissue of rats. The animals were divided into six groups: control group 1 was treated with saline as vehicle, groups 2 and 3 were treated with low and high doses of SV (100 and 500 mg/kg, respectively), group 4 was treated with LC (100 mg/kg), and groups 5 and 6 were treated with low-dose SV + LC and high-dose SV + LC, respectively. All the groups were treated orally by gastric tube for 30 successive days. Some antioxidant parameters were determined. Brain tissue (cerebral cortex) of SV-treated animals showed an increase in lipid peroxidation (LPO) and reduction in activity of enzymatic antioxidant and total antioxidant levels. Histopathological examination of cerebral cortex of SV rats showed astrocytic swelling, inflammation, and necrosis. After 4 weeks of the combination treatment of SV and LC daily, results showed significant improvement in the activity of cathepsin marker enzymes and restored the structure of the brain. LC was able to ameliorate oxidative stress deficits observed in SV rats. LC decreased LPO level and was also able to restore the activity of antioxidant enzymes as well as structural deficits observed in the brain of SV animals. The protective effect of LC in SV-treated rats is mediated through attenuation of oxidative stress, suggesting a therapeutic role for LC in individuals treated with SV.

scholarly journals GAMBARAN FAKTOR RISIKO PADA PENDERITA STROKE ISKEMIK YANG DIRAWAT INAP NEUROLOGI RSUP PROF. DR. R. D. KANDOU MANADO PERIODE JULI 2012 - JUNI 2013

e-CliniC ◽  
2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Glen Y. C. R. Kabi ◽  
Rizal Tumewah ◽  
Mieke A. H. N. Kembuan
Keyword(s):  
Risk Factors ◽  
Blood Flow ◽  
Ischemic Stroke ◽  
Brain Tissue ◽  
Tissue Damage ◽  
Medical Records ◽  
Clinical Signs ◽  
Stroke Patients ◽  
Brain Tissue Damage ◽  
The Brain

Abstract: Ischemic stroke is a clinical sign of dysfunction or brain tissue damage caused by lack of blood flow to the brain that disrupts the need for blood and oxygen to the brain. WHO defines stroke as a rapidly developing clinical signs of focal brain due to interference (or global) with symptoms - that last for 24 hours or more- and can cause death without any other obvious cause other than vascular. This study aimed to obtain an overview of risk factors in ischemic stroke patients in the Inpatient Neurology Department of Prof. Dr. R. D. Kandou Hospital Manado period July 2012 - June 2013. Data were taken by collecting data of ischemic stroke patients medical records. There were 60 patients during that period. Patients affected by stroke were aged between 51 - 65 years and had histories of hypertension.Keywords: risk factors, ischemic stroke.Abstrak: Stroke iskemik adalah tanda klinis disfungsi atau kerusakan jaringan otak yang disebabkan kurangnya aliran darah ke otak sehingga mengganggu kebutuhan darah dan oksigen di otak. WHO mendefiniskan stroke merupakan suatu tanda klinis yang berkembang cepat akibat gangguan otak fokal (atau global) dengan gejala - gejala yang berlangsung selama 24 jam atau lebih dan dapat menyebabkan kematian tanpa adanya penyebab lain yang jelas selain vaskuler. Penelitian ini bertujuan untuk mendapatkan gambaran tentang faktor resiko pada pasien stroke iskemik di rawat inap Neurologi RSUP Prof. Dr. R. D. Kandou Manado periode Juli 2012 - Juni 2013. Penelitian dilakukan dengan cara mengumpulkan data pasien yang terkena stroke iskemik di bagian rekam medik RSUP Prof. Dr. R. D. Kandou Manado. Didapatkan 60 pasiem selama periode Juli 2012 – Juni 2013. Berdasarkan hasil yang didapat maka disimpulkan bahwa pasien yang sering terkena stroke adalah pasien yang berumur antara 51-65 tahun, dan pasien yang memiliki riwayat hipertensi.Kata kunci: faktor risiko, stroke iskemik

Eugenol improves tissue damage and oxidative stress in adult female rats after ovarian torsion/detorsion

2021 ◽  
pp. 1-6
Author(s):  
Bita Barghi ◽  
Majid Shokoohi ◽  
Amir Afshin Khaki ◽  
Arash Khaki ◽  
Maryam Moghimian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adult Female ◽  
Tissue Damage ◽  
Ovarian Torsion ◽  
Female Rats ◽  
And Oxidative Stress

scholarly journals Intermittent Hypobaric Hypoxic Preconditioning Provides Neuroprotection by Increasing Antioxidant Activity, Erythropoietin Expression and Preventing Apoptosis and Astrogliosis in the Brain of Adult Rats Exposed to Acute Severe Hypoxia

2021 ◽  
Vol 22 (10) ◽  
pp. 5272
Author(s):  
Débora Coimbra-Costa ◽  
Fernando Garzón ◽  
Norma Alva ◽  
Tiago C. C. Pinto ◽  
Fernando Aguado ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hypobaric Hypoxia ◽  
Hypoxic Preconditioning ◽  
Severe Hypoxia ◽  
Efficient Tool ◽  
Adult Rats ◽  
Therapeutic Benefits ◽  
Background Exposure ◽  
The Brain ◽  
Apoptotic Cascade

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.

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.

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