Damage In Cerebral Cortex Research Articles

Investigation of the Effects of White Tea Against Cerebral Cortex Damage Induced by Cisplatin

Investigation of the Effects of White Tea Against Cerebral Cortex Damage Induced by Cisplatin

Diallyl trisulfide regulates PGK1/Nrf2 expression and reduces inflammation to alleviate neurological damage in mice after traumatic brain injury

BackgroundDiallyl trisulfide (DATS) has a direct antioxidant capacity and emerges as a promising neuroprotective agent. This study was designed to investigate the role of DATS in traumatic brain injury (TBI). MethodsTBI mouse models were established using the controlled cortical impact, followed by DATS administration. The effects of DATS on neurological deficit, brain damage, inflammation and phosphoglycerate kinase 1 (PGK1) expression were detected using mNSS test, histological analysis, TUNEL assay, enzyme-linked immunosorbent assay and immunofluorescence. PC12 cells were subjected to H2O2-induced oxidative injury after pre-treatment with DATS, followed by cell counting kit-8 assay, flow cytometry and ROS production detection. Apoptosis-related proteins and the PGK1/nuclear factor erythroid-2 related factor 2 (Nrf2) pathway were examined using Western blot. ResultsDATS ameliorated the cerebral cortex damage, neurological dysfunction and apoptosis, as well as decreased PGK1 expression and expressions of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in mice after TBI. DATS also enhanced viability, blocked apoptosis and inhibited ROS production in H2O2-induced PC12 cells. DATS downregulated Cleaved-Caspase3, Bax and PGK1 levels, and upregulated Bcl-2 and Nrf2 levels in TBI mouse models and the injured cells. ConclusionDATS regulates PGK1/Nrf2 expression and inflammation to alleviate neurological damage in mice after TBI.

Protective effects of Urtica dioica on the cerebral cortex damage induced by Potassium bromate in adult male albino rats

ABSTRACT Potassium bromate is used in cheese production, beer making and is also used in pharmaceutical and cosmetic. It is a proven carcinogen as it is a strong oxidizing agent that generates free radicals during xenobiotic metabolism. Urtica dioica (Ud) (from the plants’ family of Urticaceae) is a plant that has long been used as a medicinal plant in many parts of the world. It has been shown to have anti-inflammatory, antioxidant and immunosuppressive properties. So, this study aimed to clarify the effect of Potassium bromate on the histological structure of cerebral cortex of adult male albino rats, evaluate the possible protective role of Urtica dioica. Thirty adult healthy male albino rats were divided into three groups; group I (Control group), group II (KBrO3 treated group). Group III (KBrO3 and Urtica dioica treated group).At the end of the experiment, rats in all groups were anesthetized and specimens were processed for light and electron microscope. Morphometric and statistical analyses were also performed. Nerve cells of the treated group showed irregular contours, dark nuclei, irregular nuclear envelopes, dilated RER cisternae, and mitochondria with ruptured cristae. Vacuolated neuropil was also observed. Immunohistochemically, stained sections for GFAP showed strong positive reaction in the processes of astrocytes. Recovery group showed revealed nearly the same as the histological picture as the control group. In conclusion, potassium bromate induces degenerative effects on neurons of cerebral cortex and urtica dioica provide an important neuroprotective effects against these damaging impacts through their antioxidant properties.

ApoE isoforms alter glial Nrf2 activation, and antioxidant levels and oxidative damage in cerebral cortex of mice and humans

ApoE isoforms alter glial Nrf2 activation, and antioxidant levels and oxidative damage in cerebral cortex of mice and humans

Stem cells therapeutic effect in a reserpine-induced fibromyalgia rat model: A possible NLRP3 inflammasome modulation with neurogenesis promotion in the cerebral cortex

Fibromyalgia is a chronic pain syndrome with a multifactorial pathophysiology affecting 2–8 % of the population. AimsTo investigate the therapeutic effects of bone marrow mesenchymal stem cells (BMSCs) against fibromyalgia-related cerebral cortex damage and the possible underlying mechanisms of action. Materials and methodsRats were randomly allocated into three groups; control, fibromyalgia and fibromyalgia treated with BMSCs groups. Physical and behavioural assessments were performed. Cerebral cortices were collected for biochemical and histological assessment. Key findingsFibromyalgia group showed behavioural changes indicating presence of pain, fatigue, depression, and sleep disturbances. Moreover, biochemical biomarkers alterations were demonstrated by a significant decrease in brain monoamines and GSH levels, but MDA, NO, TNF-alpha, HMGB-1, NLRP3, and caspase-1 levels significantly increased. Furthermore, histological assessment revealed structural and ultrastructural alterations indicating neuronal and neuroglial degeneration with microglia activation, an increase in mast cell number and IL-1β immune-expression. Additionally, a significant decrease in Beclin-1 immune-expression, and blood brain barrier disruption were noticed. Interestingly, BMSCs administration significantly improved behavioural alterations, restored the reduced brain monoamines and oxidative stress markers, and reduced TNF-alpha, HMGB-1, NLRP3, and caspase-1 levels. Profoundly, cerebral cortices demonstrated improved histological structure, significant decrease in mast cell number and IL-1β immune-expression, besides a significant increase in Beclin-1 and DCX immune-expression. SignificanceFor the best of our knowledge, this is the first study showing ameliorative effects for BMSCs treatment in fibromyalgia-related cerebral cortical damage. The neurotherapeutic effects of BMSCs could be attributed to NLRP3 inflammasome signaling pathway inhibition, mast cell deactivation, and stimulation of neurogenesis and autophagy.

Medication overuse headache and substance use disorder: A comparison based on basic research and neuroimaging.

It has yet to be determined whether medication overuse headache (MOH) is an independent disorder or a combination of primary headache and substance addiction. To further explore the causes of MOH, we compared MOH with substance use disorder (SUD) in terms of the brain regions involved to draw more targeted conclusions. In this review, we selected alcohol use disorder (AUD) as a representative SUD and compared MOH and AUD from two aspects of neuroimaging and basic research. We found that in neuroimaging studies, there were many overlaps between AUD and MOH in the reward circuit, but the extensive cerebral cortex damage in AUD was more serious than that in MOH. This difference was considered to reflect the sensitivity of the cortex structure to alcohol damage. In future research, we will focus on the central amygdala (CeA), prefrontal cortex (PFC), orbital-frontal cortex (OFC), hippocampus, and other brain regions for interventions, which may have unexpected benefits for addiction and headache symptoms in MOH patients.

Paeonol Effects on Repair of Cerebral Cortex Injury and the Expression of Brain-Derived Neurotrophic Factor/Tropomyosin Receptor Kinase B in Postnatal Rats with Cerebral Palsy

Objective: To observe Paeonol effects on repair of cerebral cortex in young rats with CP. Methods: Dividing CP model rats as Model and Pae groups, and a sham operation control group was set up. Using Nissl staining to evaluate morphology and number of cortical neurons in young rats, and to determine the protein of BDNF/TrkB in peripheral serum and cerebral cortex. Results: The number of normal morphological neurons in cerebral cortex of young rats in Pae group were more than that of Model group (P < 0.01). BDNF and TrkB concentrations were significantly up-regulation in serum in Model and Pae groups (P < 0.001), meanwhile, The BDNF and TrkB concentrations significantly up-regulated in serum in Pae group (P < 0.01). By IHC and WB assay, BDNF and TrkB protein levels were significantly up-regulation in serum in Model and Pae groups (P < 0.001), meanwhile, The BDNF and TrkB protein levels were significantly up-regulation in serum in Pae group (P < 0.01). Conclusion: Pae can all play a role in repairing cerebral cortex damage in young rats with cerebral palsy via BDNF/TrkB.

N-Acetylcysteine Administration Attenuates Sensorimotor Impairments Following Neonatal Hypoxic-Ischemic Brain Injury in Rats.

Hypoxic ischemic (HI) brain injury that occurs during neonatal period has been correlated with severe neuronal damage, behavioral deficits and infant mortality. Previous evidence indicates that N-acetylcysteine (NAC), a compound with antioxidant action, exerts a potential neuroprotective effect in various neurological disorders including injury induced by brain ischemia. The aim of the present study was to investigate the role of NAC as a potential therapeutic agent in a rat model of neonatal HI brain injury and explore its long-term behavioral effects. To this end, NAC (50 mg/kg/dose, i.p.) was administered prior to and instantly after HI, in order to evaluate hippocampal and cerebral cortex damage as well as long-term functional outcome. Immunohistochemistry was used to detect inducible nitric oxide synthase (iNOS) expression. The results revealed that NAC significantly alleviated sensorimotor deficits and this effect was maintained up to adulthood. These improvements in functional outcome were associated with a significant decrease in the severity of brain damage. Moreover, NAC decreased the short-term expression of iNOS, a finding implying that iNOS activity may be suppressed and that through this action NAC may exert its therapeutic action against neonatal HI brain injury.

Disruption of the lung-gut-brain axis is responsible for cortex damage induced by pulmonary exposure to zinc oxide nanoparticles

Increasing evidence shows that gut microbiota is important for host health in response to metal nanomaterials exposure. However, the effect of gut microbiota on the cortex damage caused by pulmonary exposure to zinc oxide nanoparticles (ZnONPs) remains mainly unknown. In this study, a total of 48 adult C57BL/6J mice were intratracheally instilled with 0.6 mg/kg ZnONPs in the presence or absence of antibiotics (ABX) treatment. Besides, 24 mice were treated with or without fecal microbiota transplantation (FMT) after the intraperitoneal administration of ABX. Our results demonstrated for the first time that dysbiosis induced by ABX treatment significantly aggravated cortex damage induced by pulmonary exposure to ZnONPs. Such damage might highly occur through the induction of oxidative stress, manifested by the enhancement of antioxidative enzymes and products of lipid peroxidation. However, ferroptosis was not involved in this process. Interestingly, our data revealed that ABX treatment exacerbated the alterations of gut-brain peptides (including Sst, Sstr2, and Htr4) induced by ZnONPs in both gut and cortex tissues. Moreover, fecal microbiota transplantation (FMT) was able to alleviate cerebral cortex damage, oxidative stress, and alterations of gut-brain peptides induced by pulmonary exposure to ZnONPs. The results together indicate that pulmonary exposure to ZnONPs causes cerebral cortex damage possibly via the disruption of the lung-gut-brain axis. These findings not only propose valuable insights into the mechanism of ZnONPs neurotoxicity but also provide a potential therapeutic method against brain disorders induced by pulmonary exposure to ZnONPs. Availability of data and materialsThe datasets used and/or analyzed during the current study are available from the The corresponding author on reasonable request.

Pinus massoniana needle extracts attenuate oxidative stress injury in cerebral ischemia reperfusion rats by regulating JNK3/caspase-3 signal transduction.

To investigate the effect and mechanism of Pinus massoniana needle extracts (PNE) on oxidative stress injury in cerebral ischemia reperfusion rats. The SD male rats were randomly divided into sham group, model control group, Edaravone (3 mg/kg) group, PNE low-dose (200 mg/kg), medium-dose (400 mg/kg) and high-dose (800 mg/kg) groups. PNE was administered by gavage for 7 d before modeling and 6 h after modeling in PNE treatment groups; Edaravone was given by intraperitoneal injection 7 d before modeling and 6 h after reperfusion. The rat model of cerebral ischemia reperfusion injury was established by middle cerebral artery occlusion method. After 24 h of reperfusion, the neurological deficit score, brain water content and cerebral infarction volume of rats were measured. The pathological changes of cerebral cortex and hippocampus were observed by HE staining, and the number of normal nerve cells was counted. The apoptosis rate of neurons in cerebral cortex was detected by TUNEL method. The content of nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD) activity in ischemic brain tissue were detected. The protein expression of c-Jun N-terminal kinase (JNK) 3, phosphorylated JNK3 (p-JNK3), B-cell lymphoma protein(Bcl) -2, Bcl-2 associated X (Bax), cytochrome C and caspase-3 in cerebral cortex were detected by Western blotting method. Compared with the model control group, the behavioral score, brain water content and cerebral infarction volume in PNE groups were significantly reduced (all P<0.05), the pathological damage of cerebral cortex and hippocampal CA1 area was significantly alleviated, and the number of normal nerve cells in ischemic cortex and hippocampal CA1 area was increased (all P<0.05). The medium-dose PNE group had the best effect. Compared with the model control group, the apoptosis rate of cortical neurons, the content of NO and MDA in cerebral cortex, the ratio of p-JNK3/JNK3, the expression level of cytochrome C and caspase-3 protein in PNE medium-dose group were significantly reduced , and the activity of SOD, the Bcl-2/Bax ratio were significantly improved (all P<0.05). PNE ameliorates brain injury after cerebral ischemia reperfusion in rats, which may be related to scavenging NO and MDA, inhibiting oxidative stress-mediated JNK3/caspase-3 signsal transduction to inhibit neuronal apoptosis.

Sodium Para-aminosalicylic Acid Inhibits Lead-Induced Neuroinflammation in Brain Cortex of Rats by Modulating SIRT1/HMGB1/NF-κB Pathway.

Lead (Pb) is considered to be a major environmental pollutant and occupational health hazard worldwide which may lead to neuroinflammation. However, an effective treatment for Pb-induced neuroinflammation remains elusive. The aim of this study was to investigate the mechanisms of Pb-induced neuroinflammation, and the therapeutic effect of sodium para-aminosalicylic acid (PAS-Na, a non-steroidal anti-inflammatory drug) in rat cerebral cortex. The results indicated that Pb exposure induced pathological damage in cerebral cortex, accompanied by increased levels of inflammatory factors tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Moreover, Pb decreased the expression of silencing information regulator 2 related enzyme 1 (SIRT1) and brain-derived neurotrophic factor (BDNF), and increased the levels of high mobile group box 1 (HMGB1) expression and p65 nuclear factor-κB (NF-κB) phosphorylation. PAS-Na treatment ameliorated Pb-induced histopathological changes in rat cerebral cortex. Moreover, PAS-Na reduced the Pb-induced increase of TNF-α and IL-1β levels concomitant with a significant increase in SIRT1 and BDNF levels, and a decrease in HMGB1 and the phosphorylation of p65 NF-κB expression. Thus, PAS-Na may exert anti-inflammatory effects by mediating the SIRT1/HMGB1/NF-κB pathway and BDNF expression. In conclusion, in this novel study PAS-Na was shown to possess an anti-inflammatory effect on cortical neuroinflammation, establishing its efficacy as a potential treatment for Pb exposures.

Alantolactone reduced neuron injury via activating PI3K/Akt signaling pathway after subarachnoid hemorrhage in rats.

Subarachnoid hemorrhage (SAH) is a common disease with high morbidity and mortality, which can cause pathological, physiological, and biological reactions. SAH causes a series of responses such as neuronal and cerebral cortex damage, which in turn leads to inflammation and apoptosis. Traditional Chinese medicine has a strong anti-inflammatory effect, such as Alantolactone (ATL). However, studies on ATL therapy for SAH have not been reported. We observed the neurological scores, brain water content, Evans blue (EB) extravasation, neuroinflammation, and apoptosis via performing an enzyme-linked immunosorbent assay (ELISA), western blotting, immunofluorescence staining, and other methods after SAH. In this study, we found that ATL treatment attenuated the neurologic deficits, inhibited neuronal apoptosis and inflammatory reaction, promoted polarization of microglia toward the M2 phenotype, and activated the PI3K/Akt signaling pathway. ATL can reduce the neurons and cerebral cortex damage of SAH rats through activating PI3K/Akt signaling pathway.

Cheyne–Stokes respiration in two sheep during recovery from general anaesthesia for experimental convection enhanced drug delivery

AbstractTwo 8‐month‐old Suffolk sheep, weighing 45 and 55 kg, respectively, were anaesthetised for an intrathalamic injection of an experimental drug. After an uneventful procedure and general anaesthesia using controlled mechanical ventilation, the sheep were weaned off the ventilator and allowed to breathe spontaneously with end‐tidal carbon dioxide (PE′CO2) levels remaining within normal limits. During recovery, intermittent apnoeic phases were observed with increasing PE′CO2 (&gt;70 mmHg) and decreasing oxygen saturation of haemoglobin (SpO2) levels (90%–91%). The sheep appeared unresponsive, and reflexes were absent. This alternated with phases of normal mentation, normal reflexes and regular spontaneous ventilation, where ventilatory parameters improved. Tentative treatment to reduce intracranial pressure and administration of the opioid receptor antagonist naloxone were unsuccessful. Definite diagnosis of Cheyne–Stokes respiration is difficult but was suspected in these two cases; cerebral cortex damage, intracranial haemorrhage or opioid mediated respiratory rhythm disturbances are possible causes.

Long-term exposure to ephedrine leads to neurotoxicity and neurobehavioral disorders accompanied by up-regulation of CRF in prefrontal cortex and hippocampus in rhesus macaques

Drug addiction continues to threaten the health and welfare of people worldwide, and ephedrine abuse is a serious drug problem in many areas of the world. Ephedrine toxicity is thought to induce behavioral effects primarily through actions on the central nervous system. The corticotropin-releasing factor (CRF) system plays an important role in regulating behavioral effects induced by addictive drugs, but whether CRF is related to ephedrine toxicity remains unclear. This study seeks to examine whether there is a correlation between the CRF and chronic ephedrine neurotoxicity. To this end, we established a chronic ephedrine (0.4–1.6 mg/kg/d) exposure model in rhesus macaques, assessed its effects on body weight and behavior, examined neuronal changes in the prefrontal cortex and hippocampus, and measured the CRF expression in the prefrontal cortex and hippocampus. After 8-weeks of exposure to ephedrine, the toxic effects of ephedrine included significant weight loss and induction of behavioral changes in rhesus macaques. In particular, in the modeling group, the abnormal behavioral changes mainly manifested as irritability and behavioral sensitization. Meanwhile, the histological abnormalities included neuronal morphological changes, pyknosis and irregular shapes of neurons in the prefrontal cortex and hippocampus. In addition, the expression levels of CRF mRNA and protein were increased in the prefrontal cortex and hippocampus of ephedrine-treated animals. In summary, the finding of this study indicated that ephedrine neurotoxicity can cause neuronal damage in cerebral cortex, which in turn can result in certain neurobehavioral abnormalities, and that CRF expression in prefrontal cortex and hippocampus is elevated in response to ephedrine exposure. These observations suggested that long-term exposure to ephedrine might be causing neurotoxicity and leading to neurobehavioral disorders accompanied by up-regulation of CRF in prefrontal cortex and hippocampus.

Multi metric functional connectivity analysis based on continuous hidden Markov model with application in early diagnosis of Alzheimer’s disease

Functional connectivity (FC) is referred to as statistical dependencies between regions of interest. To investigate brain functional connectivity, there are many different connectivity metrics and researches show that the choice of the connectivity metric influences the results of the study and there is no golden rule of choosing the best connectivity metric.It is assumed that functional connectivity has a neural basis, and therefor is related to a variety of different neurological disorders like Alzheimer’s disease (AD) and Parkinson. AD is the most common neurodegenerative disorder. Cerebral cortex damage and synaptic plasticity disturbance in AD cause a decrease in functional connectivity. Mild Cognitive Impairment (MCI) is the first stage in AD progression and causes measurable decline in memory and cognitive abilities.In this study, a novel methodology is presented to combine several connectivity metrics with the goal of improving between-class discrimination. In the proposed method, temporal changes of multiple functional connectivity metrics are investigated along sliding windows by modeling it as the observation vector of a continuous observation hidden Markov model (HMM). The performance of the proposed method is evaluated using resting state eyes-closed EEG data from 7 MCI patients and 7 age-matched normal controls (NC).Group differences were investigated in five different frequency bands: delta, theta, alpha, beta, and gamma. Method analysis revealed that NC subjects and MCI patients are discriminated with accuracy of %95.9 ± 0.4 and %97.2 ± 0.5 over the alpha and gamma frequency bands respectively, using leave one subject out cross validation. These results indicate the proficiency of the connectivity metrics combination in distinguishing MCI from NC.

Identification of proteins differentially expressed by glutamate treatment in cerebral cortex of neonatal rats

Glutamate leads to neuronal cell damage by generating neurotoxicity during brain development. The objective of this study is to identify proteins that differently expressed by glutamate treatment in neonatal cerebral cortex. Sprague-Dawley rat pups (post-natal day 7) were intraperitoneally injected with vehicle or glutamate (10 mg/kg). Brain tissues were isolated 4 h after drug treatment and fixed for morphological study. Moreover, cerebral cortices were collected for protein study. Two-dimensional gel electrophoresis and mass spectrometry were carried out to identify specific proteins. We observed severe histopathological changes in glutamate-exposed cerebral cortex. We identified various proteins that differentially expressed by glutamate exposure. Identified proteins were thioredoxin, peroxiredoxin 5, ubiquitin carboxy-terminal hydrolase L1, proteasome subunit alpha proteins, isocitrate dehydrogenase, and heat shock protein 60. Heat shock protein 60 was increased in glutamate exposed condition. However, other proteins were decreased in glutamate-treated animals. These proteins are related to anti-oxidant, protein degradation, metabolism, signal transduction, and anti-apoptotic function. Thus, our findings can suggest that glutamate leads to neonatal cerebral cortex damage by regulation of specific proteins that mediated with various functions.

LncRNA Lethe protects sepsis-induced brain injury via regulating autophagy of cortical neurons.

To investigate the role of long non-coding RNA (lncRNA) Lethe in mediating autophagy of cortical neurons in mice with sepsis-induced brain injury (SIBI). A total of 60 wild-type C57BL/6 mice were divided into sham-operated wild-type (SWT) group and wild-type model (MWT) group. Sixty Lethe-/- mice were divided into sham-operated knockout (SKO) group and model knockout (MKO) group. Each group had 30 mice. Sepsis model in mice was established by cecal ligation and puncture (CLP). Neurobiological score was recorded at 6 h after CLP. Mice with lower than 6 scores of neurobehavioral tests were diagnosed with SIBI. Quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to determine mRNA levels of Lethe and interferon-γ (INF-γ) in cortical neurons of SIBI mice. Western blot was conducted to detect protein levels of LC3-II, LC3-I and SQSTM1 in mice. Neuronal impairment in mouse brain was evaluated by hematoxylin and eosin (HE) staining. Expressions of LC3-I and LC3-II in cerebral cortex of MWT group began to increase at 6 h after CLP, and remained at high levels until 96 h. On the contrary, SQSTM1 expression in cerebral cortex of MWT group began to decrease at 6 h after CLP. Compared with SWT group, expressions of Lethe and IFN-γ were remarkably upregulated in cortex of MWT group at 12 h after CLP. Expression of LC3-II in MWT group was remarkably upregulated, while SQSTM1 was downregulated at 12 h after CLP, which were contrary to those in MKO group. At 12 h after CLP, the neurobiological scores of the MKO group (4.97±0.71) were markedly lower than those of the MWT group (5.43±0.86). HE staining showed worse damage in cerebral cortex and fewer neurons of MKO group relative to MWT group. Lethe has a protective effect on SIBI mice by regulating autophagy in mouse cortical neurons.

Baicalin attenuates lipopolysaccharide-induced neuroinflammation in cerebral cortex of mice via inhibiting nuclear factor kappa B (NF-κB) activation.

Baicalin is a plant-derived flavonoid that has anti-inflammatory and anti-oxidative effects. We investigated an anti-inflammatory effect of baicalin against lipopolysaccharide (LPS)-induced damage in cerebral cortex. Adult mice were divided into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 µg/kg/day) and baicalin (10 mg/kg/day) were intraperitoneally injected for 7 days. LPS treatment induced histopathological changes in cerebral cortex, whereas baicalin protected neuronal cells against LPS toxicity. Moreover, baicalin treatment attenuated LPS-induced increases of reactive oxygen species and oxidative stress in cerebral cortices. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are known as markers of activated microglia and astrocyte, respectively. Results of Western blot and immunofluorescence staining showed that LPS exposure induces increases of Iba-1 and GFAP expressions, whereas baicalin alleviates LPS-induced increases of these proteins. Baicalin also prevented LPS-induced increase of nuclear factor kappa B (NF-κB). LPS treatment led to increases of pro-inflammatory factors including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these pro-inflammatory mediators were attenuated in baicalin co-treated animals. These results demonstrated that baicalin regulates neuroglia activation and modulates inflammatory factors in LPS-induced neuronal injury. Thus, our findings suggest that baicalin exerts a neuroinflammatory effect against LPS-induced toxicity through decreasing oxidative stress and inhibiting NF-κB mediated inflammatory factors, such as IL-1β and TNF-α.

Cerebral cortex damage induced by acute oral alcohol intake is associated with oxidative stress in Wistar rats (Rattus norvegicus)

The prefrontal cortex undergoes functional and structural changes due to binge or chronic alcohol consumption. This study examines alcohol-induced cerebral cortex damage and the association with oxidative stress in an animal model. Twenty-four Wistar rats (12 males and 12 females) weighing 150g to 250g were divided into four groups, A, B, C and D according to their weights. The rats in groups B, C and D were administered with 2mls of 52.5%, 16.5% and 4.3% v/v aqueous alcoholic solution respectively for 21 days. While rats in group A (control group) were given distilled water only, for the same period. The brain of each rat was excised, weighed and fixed in 10% formal saline for histological analysis while others were immersed in ice cold 30% sucrose solution, homogenized and analyzed for superoxide dismutase, malondialdehyde and acetylcholinesterase activity. Results indicate chromatolysis of Nissl bodies, cortical necrosis, and uneven neuronal loss with varying range of vacuolations in the prefrontal cortices of the alcohol treated rats in a dosedependent manner when compared with the control group. Cerebral cortex damage due to acute oral alcohol intake is associated with oxidative stress.Keywords: Brain, cerebral cortex, alcohol, Wistar rats, oxidative stress

Manual acupuncture improves parameters associated with oxidative stress and inflammation in PTZ-induced kindling in mice.

The use of acupuncture in the treatment of central nervous system (CNS) disorders is an age-old practice. Although only a few studies have proved its efficacy, evidence has indicated the use of acupuncture to treat different types of seizures. Therefore, the present study aimed to evaluate the effect of manual acupuncture (MAC) using the chemical kindling model. The role of MAC in oxidative stress and inflammation after pentylenetetrazole (PTZ)-induced kindling was investigated by measuring reactive oxygen species (ROS) production, superoxide dismutase (SOD), and catalase (CAT) activities, nitrite content, and deoxyribonucleic acid (DNA) damage in cerebral cortex. Mice received PTZ (60mg/kgs.c.) once every three days for 16days, totaling six treatments. MAC was applied at acupoint GV20 daily during the entire experimental protocol. Diazepam (DZP) (2mg/kg) was used as positive control. Also, we evaluated the MAC effect associated with DZP (MAC/DZP) at a low dose (0.15mg/kg). The results demonstrated that MAC or MAC/DZP were not able to reduce significantly seizure occurrence or to increase the latency to the first seizure during treatment. MAC/DZP promoted a difference in the first latency to seizure only on the third day. PTZ-induced kindling caused significant neuronal injury, oxidative stress, increased DNA damage, nitric oxide production, and expression of the pro-inflammatory Tumor Necrosis Factor-α (TNF-α). These effects were reversed by treatment with MAC or MAC/DZP. These results indicated that the stimulation of acupoint GV20 by MAC showed no potential antiepileptogenic effect in the model used, although it greatly promoted neuronal protection, which may result from antioxidant and anti-inflammatory effects observed here.