scholarly journals Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Depeng Feng ◽  
Dezhe Chen ◽  
Tuanzhi Chen ◽  
Xiaoqian Sun
Keyword(s):  
Matrix Metalloproteinase ◽  
Test Scores ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Cerebral Injury ◽  
Control Group ◽  
Secondary Brain Injury ◽  
Walking Test ◽  
Matrix Metalloproteinase 3 ◽  
Injured Brain

Objective. This study is aimed at exploring the possible neuroprotective mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. Methods. We established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, the injured brain area, and the beam walking test were used to estimate the degree of cerebral injury among the rats. Immunohistochemistry and immunofluorescence were used to detect activated microglia, matrix metalloproteinase-3 (MMP-3), and osteopontin (OPN). Results. The injured brain area and mortality were dramatically reduced ( p < 0.01 ), and the beam walking test scores were elevated ( p < 0.01 ) in the acetylsalicylic acid (ASA) group compared to the control group. The number of microglia-, MMP-3-, and OPN-positive cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group. After LPS stimulation, the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. In the ASA group, the number of microglia was significantly smaller ( p < 0.05 ), especially at 24 h ( p < 0.01 ), compared to the LPS group. Moreover, the injured brain area and the mortality were dramatically increased and the beam walking test scores were reduced ( p < 0.01 ) after LPS simulation following CIRP. The degree of injury in the ASA group resembled that in the control group. However, the number of MMP-3-immunoreactive neurons or microglia was significantly larger than that of the control group ( p < 0.05 ). In the ASA group, the MMP-3 expression was also considerably decreased ( p < 0.05 ). Conclusions. After CIRP, microglia were rapidly activated and the expression of MMP-3 and OPN significantly increased. For rats injected with LPS at reperfusion, the injured brain area and mortality also dramatically increased and the neurologic impairment worsened. However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction after CIRP injury.

Neurophysiologic Monitoring and Neuroprotection

2017 ◽  
Author(s):  
Aws Alawi ◽  
Michael Reznik ◽  
Jan Claassen
Keyword(s):  
Early Detection ◽  
Brain Injuries ◽  
Cerebral Injury ◽  
Secondary Brain Injury ◽  
Neurophysiologic Monitoring ◽  
Permanent Damage ◽  
Injured Brain ◽  
Physiological Assessment ◽  
Physiologic Parameters ◽  
Sedation Monitoring

One of the main goals of monitoring neurologically ill patients is detection of secondary brain injury early enough to intervene to prevent permanent damage. In some patients with impaired levels of consciousness and those who require sedation, monitoring various brain physiologic parameters by invasive and noninvasive means has become an essential tool in the care of critically ill patients. Integration of multiple physiological parameters provides a more comprehensive physiological assessment of the injured brain and allows real-time, early detection of secondary cerebral injury and intervention to prevent permanent damage. Importantly, these modalities should be interpreted collectively and not in isolation in order to manage acute brain injuries, which are often complex and dynamic at the same time.

scholarly journals Relationship of matrix metalloproteinase-3 -11715A/6A polymorphism (rs35068180) and dilated cardiomyopathy

2020 ◽  
Vol 25 (10) ◽  
pp. 3960
Author(s):  
S. Yu. Nikulina ◽  
O. O. Kuznecova ◽  
A. A. Chernova ◽  
V. N. Maksimov
Keyword(s):  
Matrix Metalloproteinase ◽  
Unknown Etiology ◽  
Control Group ◽  
General Direction ◽  
Matrix Metalloproteinase 3 ◽  
Arterial Walls ◽  
Idiopathic Cardiomyopathy ◽  
The Mean ◽  
Relationship Of ◽  
The Relationship

Aim. To study the relationship of matrix metalloproteinase-3 (MMP3) genetic polymorphism and dilated ischemic cardiomyopathy (DCM), as well as idiopathic cardiomyopathy (ICM) of unknown etiology.Material and methods. A total of 221 patients with DCM and ICM were examined (mean age, 55,30±9,69 years). The group of ischemic DCM consisted of 111 people (99 men (89,2%) and 12 women (10,8%)). The mean age of DCM subjects was 51,73±9,74 years (male subgroup, 51,00±8,96 years; female subgroup, 57,75±3,71 years). The ICM group consisted of 110 people (100 men (91,5%) and 10 women (8.5%)). The mean age of ICM subjects was 58,68±8.38 years (male subgroup, 58,29±8.,6 years; female subgroup, 62,90±6,29 years). The control group of subjects (n=121) consisted of healthy people without cardiovascular diseases (mean age, 53,6±4,8 years). All patients of the experimental group underwent routine diagnostic tests, as well as coronary angiography. In case of suspected myocarditis, cardiac magnetic resonance imaging was performed. All patients underwent polymerase chain reaction to determine the MMP3-11715A/6A polymorphism (rs35068180).Results. In patients with cardiomyopathy, regardless of the disease origin, significant differences were verified in comparison with the control group. Allele 6A (65,8% vs 59,3%, p=0,044) and genotype 6A/6A (42,1% vs 32,6%, p=0,099) were found significantly more frequently in patients with cardiomyopathy than in the control group. In addition, despite various etiological factors, the pathogenetic involvement of MMP3 is likely to have a general direction.Conclusion. In all patients with cardiomyopathy, the prevalence of MMP3 gene A allele was shown. Due to decrease in the transcription activity in homozygous 6A allele, the stromelysin level in arterial walls also decreases. This promotes the activation of procollagenase-1, the deposition of extracellular matrix and cardiac remodeling

scholarly journals Does Matrix Metalloproteinase-3 Polymorphism Play a Role in Age-Related Macular Degeneration in Patients With Myocardial Infarction?

Medicina ◽  
2012 ◽  
Vol 48 (8) ◽  
pp. 60 ◽  
Author(s):  
Rasa Liutkevičienė ◽  
Diana Žaliaduonytė-Pekšienė ◽  
Dalia Žaliūnienė ◽  
Olivija Gustienė ◽  
Vytautas Jašinskas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Gene Polymorphism ◽  
Matrix Metalloproteinase ◽  
Macular Degeneration ◽  
Early Stage ◽  
Gene Promoter ◽  
Age Related Macular Degeneration ◽  
Control Group ◽  
Matrix Metalloproteinase 3 ◽  
Age Related

Objective. The aim of our study was to determine if the genotype of the matrix metalloproteinase- 3 (MMP-3) gene might carry the risk of age-related macular degeneration (ARMD) in patients with myocardial infarction. Material and Methods. A total of 499 patients with an acute myocardial infarction or with a history of myocardial infarction were enrolled into the study. They were subdivided into 2 groups: 273 patients with ARMD and 226 patients without ARMD. The control group comprised 560 persons from a random sample of the Lithuanian population. DNA was analyzed using real-time polymerase chain reaction to genotype polymorphism 5A/6A at a position –1171 of the MMP-3 gene promoter. Results. Of the 499 patients with myocardial infarction, 47% had early-stage ARMD. The patients with ARMD were older than the patients in the group without ARMD (62.1±10.8 vs. 59.6±11.1, P<0.01). The analysis of MMP-3 gene polymorphism did not reveal any differences in the distribution of 5A/5A, 5A/6A, and 6A/6A genotypes between the ARMD group, non-ARMD group, and the control group (24.2%, 52.5%, and 23.3% in the ARMD group; 28.7%, 51.9%, and 19.4% in non-ARMD group; and 25.7%, 49.3% and 25.0%, in the control group, respectively). Conclusions. MMP-3 gene polymorphism had no predominant effect on the development of ARMD in patients with myocardial infarction.

scholarly journals Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guangqian Li ◽  
LeiQian ◽  
Pan Gu ◽  
Dan Fan
Keyword(s):  
Cardiac Arrest ◽  
Neuroprotective Effect ◽  
Serum Levels ◽  
Spontaneous Circulation ◽  
Cerebral Injury ◽  
Control Group ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Neuroprotective Effects ◽  
Return Of Spontaneous Circulation

Abstract Background Neuroprotection strategies after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR) remain key areas of basic and clinical research. This study was designed to investigate the neuroprotective effects of dexmedetomidine following resuscitation and potential mechanisms. Methods Anesthetized rats underwent 6-min asphyxia-based cardiac arrest and resuscitation, after which the experimental group received a single intravenous dose of dexmedetomidine (25 μg/kg). Neurological outcomes and ataxia were assessed after the return of spontaneous circulation. The serum levels and brain expression of inflammation markers was examined, and apoptotic cells were quantified by TUNEL staining. Results Neuroprotection was enhanced by dexmedetomidine post-conditioning after the return of spontaneous circulation. This enhancement was characterized by the promotion of neurological function scores and coordination. In addition, dexmedetomidine post-conditioning attenuated the serum levels of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α at 2 h, as well as interleukin IL-1β at 2, 24, and 48 h. TUNEL staining showed that the number of apoptotic cells in the dexmedetomidine post-conditioning group was significantly reduced compared with the control group. Further western blot analysis indicated that dexmedetomidine markedly reduced the levels of caspase-3 and nuclear factor-kappa B (NF-κB) in the brain. Conclusions Dexmedetomidine post-conditioning had a neuroprotective effect against cerebral injury following asphyxia-induced cardiac arrest. The mechanism was associated with the downregulation of apoptosis and neuroinflammation.

scholarly journals Neuroprotective Effect of Mild Hypothermia in Patients Undergoing Coronary Artery Surgery With Cardiopulmonary Bypass

Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Howard J. Nathan ◽  
George A. Wells ◽  
Janet L. Munson ◽  
Denise Wozny
Keyword(s):  
Cardiopulmonary Bypass ◽  
Coronary Artery ◽  
Mild Hypothermia ◽  
Neuroprotective Effect ◽  
Cognitive Outcome ◽  
Cerebral Injury ◽  
Control Group ◽  
Coronary Artery Surgery ◽  
Neuroprotective Strategy ◽  
Hypothermic Group

Background Neuropsychological deficits occur in 30% to 80% of patients undergoing heart surgery and are due in part to ischemic cerebral injury during cardiopulmonary bypass. We tested whether mild hypothermia, the most efficacious neuroprotective strategy found in laboratory studies, improved cognitive outcome in patients undergoing coronary artery surgery. Methods and Results Patients 60 years or older scheduled for coronary artery surgery were enrolled. During cardiopulmonary bypass, patients were initially cooled to 32°C then randomly assigned to rewarming to 37°C (control) or 34°C (hypothermic), with no further intraoperative warming. Testing was scheduled preoperatively and 1 week and 3 months postoperatively. Eleven tests were combined into 3 cognitive domains: memory, attention, and psychomotor speed and dexterity. A patient was classified as having a cognitive deficit if a decrease of ≥0.50 SD was realized in 1 or more domains. The incidence of cognitive deficits 1 week after surgery, which was the primary outcome, was 62% ( \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\frac{62}{100}\) \end{document} ) in the control group and 48% ( \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\frac{45}{94}\) \end{document} ) in the hypothermic group (relative risk 0.77, P =0.048). In the hypothermic group, the magnitude of deterioration in attention and in speed and dexterity was reduced by 55.6% ( P =0.038) and 41.3% ( P =0.042), respectively. At 3 months, the hypothermic group still performed better on one test of speed and dexterity (grooved pegboard). There was no difference in morbidity or mortality. Conclusions Our findings support a neuroprotective effect of mild hypothermia in patients undergoing coronary artery surgery and should encourage physicians and perfusionists to pay careful attention to brain temperature during cardiopulmonary bypass.

scholarly journals Possible Association Between DHEA and PKCε in Hepatic Encephalopathy Amelioration: A Pilot Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Alessandro Di Cerbo ◽  
Luca Roncati ◽  
Carlotta Marini ◽  
Gianluca Carnevale ◽  
Manuela Zavatti ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Control Group ◽  
Sprague Dawley ◽  
Kinase C ◽  
Sprague Dawley Rats ◽  
Protein Kinase C Epsilon ◽  
Neuronal Functions ◽  
And Control

Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by liver failure and by an impaired neurotransmission and neurological function caused by hyperammonemia (HA). HE, in turn, decreases the phosphorylation of protein kinase C epsilon (PKCε), contributing to the impairment of neuronal functions. Dehydroepiandrosterone (DHEA) exerts a neuroprotective effect by increasing the GABAergic tone through GABAA receptor stimulation. Therefore, we investigated the protective effect of DHEA in an animal model of HE, and the possible modulation of PKCε expression in different brain area.Methods: Fulminant hepatic failure was induced in 18 male, Sprague–Dawley rats by i.p. administration of 3 g/kg D-galactosamine, and after 30 min, a group of animals received a subcutaneous injection of 25 mg/kg (DHEA) repeated twice a day (3 days). Exploratory behavior and general activity were evaluated 24 h and 48 h after the treatments by the open field test. Then, brain cortex and cerebellum were used for immunoblotting analysis of PKCε level.Results: DHEA administration showed a significant improvement of locomotor activity both 24 and 48 h after D-galactosamine treatment (****p &lt; 0.0001) but did not ameliorate liver parenchymal degeneration. Western blot analysis revealed a reduced immunoreactivity of PKCε (*p &lt; 0.05) following D-galactosamine treatment in rat cortex and cerebellum. After the addition of DHEA, PKCε increased in the cortex in comparison with the D-galactosamine-treated (***p &lt; 0.001) and control group (*p &lt; 0.05), but decreased in the cerebellum (*p &lt; 0.05) with respect to the control group. PKCε decreased after treatment with NH4Cl alone and in combination with DHEA in both cerebellum and cortex (****p &lt; 0.0001). MTS assay demonstrated the synergistic neurotoxic action of NH4Cl and glutamate pretreatment in cerebellum and cortex along with an increased cell survival after DHEA pretreatment, which was significant only in the cerebellum (*p &lt; 0.05).Conclusion: An association between the DHEA-mediated increase of PKCε expression and the improvement of comatose symptoms was observed. PKCε activation and expression in the brain could inhibit GABA-ergic tone counteracting HE symptoms. In addition, DHEA seemed to ameliorate the symptoms of HE and to increase the expression of PKCε in cortex and cerebellum.

scholarly journals Dexmedetomidine postconditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

2020 ◽  
Author(s):  
Dan Fan ◽  
GuangQian Li ◽  
Lei Qian ◽  
Pan Gu
Keyword(s):  
Cardiac Arrest ◽  
Neuroprotective Effect ◽  
Serum Levels ◽  
Spontaneous Circulation ◽  
Cerebral Injury ◽  
Control Group ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Down Regulation ◽  
Return Of Spontaneous Circulation

Abstract Background and Purpose Neuroprotection strategies after cardiac arrest (CA)/cardiopulmonary resuscitation (CPR) remain key areas of basic and clinical research. This study was designed to investigate the neuroprotective effects of dexmedetomidine following resuscitation and potential mechanisms. Methods Anesthetized rats underwent 6-minute asphyxia-based cardiac arrest and resuscitation, after which the experimental group received a single intravenous dose of dexmedetomidine (25μg/kg). Neurological outcomes and ataxia were assessed after the return of spontaneous circulation. The serum levels and brain expression of inflammation markers was examined, and apoptotic cells were quantified by TUNEL staining. Results Neuroprotection was enhanced by dexmedetomidine post-conditioning after the return of spontaneous circulation. This enhancement was characterized by the promotion of survival, neurological function scores and coordination. In addition, dexmedetomidine post-conditioning attenuated the serum levels of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α at 2h, as well as interleukin (IL)-6 at 2, 24, and 48h. TUNEL staining showed that the number of apoptotic cells in the dexmedetomidine post-conditioning group was significantly reduced compared with in the control group. Further western blot analysis indicated that dexmedetomidine markedly reduced the levels of caspase-3 and nuclear factor-kappa B (NF-κB) in the brain. Conclusions Dexmedetomidine post-conditioning had a neuroprotective effect against cerebral injury following asphyxia-induced cardiac arrest and improved the survival rate. The mechanism was associated with the down-regulation of apoptosis and neuroinflammation.

scholarly journals MiR-22-3p Expression is down-regulated in lung adenocarcinoma

2021 ◽  
Author(s):  
Dong-Jie Ma ◽  
Xiao-Yun Zhou ◽  
Ying-Zhi Qin ◽  
Zhen-Huan Tian ◽  
Hong-Sheng Liu ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Lung Adenocarcinoma ◽  
Time Correlation ◽  
Clinicopathological Characteristics ◽  
Immunohistochemical Method ◽  
Maximum Diameter ◽  
Normal Lung ◽  
Control Group ◽  
Matrix Metalloproteinase 3 ◽  
Significant Difference

Background: Our current study was performed with an attempt to detect the expression of microRNA-22-3p (miR-22-3p) in lung adenocarcinoma, as well as to analyze its role in clinical practice. In addition, its relationship with vascular endothelial growth factor (VEGF) and metastasis related indexes was focused. Material and Method: The trials in which 62 cases of lung adenocarcinoma were received to collect tumor tissue (study group) and normal lung tissue (control group) were eligible for this study. The expression of miR-22-3p in the two groups was detected through RT-PCR. Immunohistochemical method was used to detect the expression of VEGF and leukocyte differentiation antigen 31 (CD31) marked microvessel density (MVD) in lung adenocarcinoma. The expressions of matrix metalloproteinase-3 (MMP-3) and matrix metalloproteinase-7 (MMP-7) in lung adenocarcinoma were also detected through the use of Western Blot. Results: The present study revealed significant difference in the expression of miR-22-3p between the two groups. No significant difference in the expression of gender, age, neural invasion and the number of lesions were observed between groups. There was significant difference in the expression of miR-22-3p in the maximum diameter of tumor, pleural recidivism, vascular recidivism, lymph node metastasis and different TNM stages. Based on survival analysis, miR-22-3p was linked to survival time. Correlation analysis indicated that there was negative correlation between miR-22-3p and VEGF, miR-22-3p and MVD, miR-22-3p and MMP-3, and miR-22-3p and MMP-7 in lung adenocarcinoma. Conclusion: Our findings provide evidence that miR-22-3p is low expressed in lung adenocarcinoma tissues and the low expression of miR-22-3p is closely associated with clinicopathological characteristics and the prognosis. MiR-22-3p may be involved in the tumor progression of lung adenocarcinoma and may serve as a biomarker for the diagnosis and prognosis of lung adenocarcinoma.

scholarly journals Increased Sample Entropy in EEGs During the Functional Rehabilitation of an Injured Brain

Entropy ◽  
2019 ◽  
Vol 21 (7) ◽  
pp. 698 ◽  
Author(s):  
Qiqi Cheng ◽  
Wenwei Yang ◽  
Kezhou Liu ◽  
Weijie Zhao ◽  
Li Wu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Sham Group ◽  
Brain Area ◽  
Recovery Process ◽  
Sample Entropy ◽  
Control Group ◽  
Functional Rehabilitation ◽  
Injured Brain ◽  
Injury Group ◽  
Neural Remodeling

Complex nerve remodeling occurs in the injured brain area during functional rehabilitation after a brain injury; however, its mechanism has not been thoroughly elucidated. Neural remodeling can lead to changes in the electrophysiological activity, which can be detected in an electroencephalogram (EEG). In this paper, we used EEG band energy, approximate entropy (ApEn), sample entropy (SampEn), and Lempel–Ziv complexity (LZC) features to characterize the intrinsic rehabilitation dynamics of the injured brain area, thus providing a means of detecting and exploring the mechanism of neurological remodeling during the recovery process after brain injury. The rats in the injury group (n = 12) and sham group (n = 12) were used to record the bilateral symmetrical EEG on days 1, 4, and 7 after a unilateral brain injury in awake model rats. The open field test (OFT) experiments were performed in the following three groups: an injury group, a sham group, and a control group (n = 10). An analysis of the EEG data using the energy, ApEn, SampEn, and LZC features demonstrated that the increase in SampEn was associated with the functional recovery. After the brain injury, the energy values of the delta1 bands on day 4; the delta2 bands on days 4 and 7; the theta, alpha, and beta bands and the values of ApEn, SampEn, and LZC of the cortical EEG signal on days 1, 4 and 7 were significantly lower in the injured brain area than in the non-injured area. During the process of recovery for the injured brain area, the values of the beta bands, ApEn, and SampEn of the injury group increased significantly, and gradually became equal to the value of the sham group. The improvement in the motor function of the model rats significantly correlated with the increase in SampEn. This study provides a method based on EEG nonlinear features for measuring neural remodeling in injured brain areas during brain function recovery. The results may aid in the study of neural remodeling mechanisms.

scholarly journals Histopathological and Biochemical Assessment of Neuroprotective Effects of Sodium Valproate and Lutein on the Pilocarpine Albino Rat Model of Epilepsy

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Aziza Rashed Al-Rafiah ◽  
Khlood Mohammed Mehdar
Keyword(s):  
Oxidative Stress ◽  
Sodium Valproate ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Latency Period ◽  
Cerebral Injury ◽  
Control Group ◽  
Rotarod Performance ◽  
Group I ◽  
Anti Inflammatory

Epilepsy is one of the most frequent neurological disorders characterized by an enduring predisposition to generate epileptic seizures. Oxidative stress is believed to directly participate in the pathways of neurodegenerations leading to epilepsy. Approximately, one-third of the epileptic patients who suffer from seizures do not receive effective medical treatment. Sodium valproate (SVP) is a commonly used antiepileptic drug (AED); however, it has toxic effects. Lutein (L), a carotenoid, has potent antioxidant and anti-inflammatory properties. The aim of this study was to determine the neuroprotective effect of sodium valproate (SVP) and lutein (L) in a rat model of pilocarpine- (PLC-) induced epilepsy. To achieve this aim, fifty rats were randomly divided into five groups. Group I: control, group II: received PLC (400 mg/kg intraperitoneally), group III: received PLC + SVP (500 mg/kg orally), group IV: received PLC + SVP + L (100 mg/kg orally), and group V: received (PLC + L). Racine Scale (RC) and latency period to onset seizure were calculated. After eight weeks, the hippocampus rotarod performance and histological investigations were performed. Oxidative stress was investigated in hippocampal homogenates. Results revealed that SVP and L, given alone or in combination, reduced the RC significantly, a significant delay in latency to PLC-kindling onset, and improved rotarod performance of rats compared with the PLC group. Moreover, L was associated with a reduction of oxidative stress in hippocampal homogenate, a significant decrease in serum tumor necrosis factor-alpha (TNF-α) level, and inhibition of cerebral injury and displayed antiepileptic properties in the PLC-induced epileptic rat model. Data obtained from the current research elucidated the prominent neuroprotective, antioxidant, and anti-inflammatory activities of lutein in this model. In conclusion, lutein cotreatment with AEDs is likely to be a promising strategy to improve treatment efficacy in patients suffering from epilepsy.

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