Rat Brain Tissue Research Articles

Investigation of the Effects of Light, Darkness, and Dim Light on Rat Brain Tissue: A Biochemical and Histological Study.

This study evaluates acetylcholinesterase (AChE) enzyme activity levels, oxidative stress parameters, histopathological findings, and serum melatonin levels in rat brain tissue. 32 male Wistar Albino rats were randomly divided into four groups: Control, Light, Dark, Dim light (n = 8 each group). After a 30 day experiment, brain tissues were collected to measure AChE, glutathione S-transferase (GST), glutathione (GSH), and malondialdehyde (MDA) levels and conduct histopathological analyses. Serum melatonin levels were also measured. In this study, we observed a significant increase in MDA levels in dim light, dark, and light groups. AChE and α-GST enzyme activity levels were significantly decreased in the dark group compared with the other groups. Additionally, there was a statistical difference in melatonin levels between the light and dark groups. In the light microscope examination of the sections stained with hematoxylin-eosin from the dark group brain tissue, mild perineuronal edema was observed in all areas. Our study is the first to compare the effects of three groups on the brain: continuous light, continuous darkness, and dim light at night. Additionally, it is the only study to examine the effects of light exposure differences on the brain AChE levels.

Electroacupuncture combined with trigonelline inhibits pyroptosis in cerebral ischemia-reperfusion by suppressing autophagy via the PI3K/AKT/mTOR signaling pathway.

Electroacupuncture (EA) and trigonelline (TG) have been reported to be beneficial in alleviating cerebral ischemia/reperfusion injury (CIRI). However, the synergistic effects of EA and TG in CIRI and the underlying mechanism have not been demonstrated. Rats were subjected to middle cerebral artery occlusion (MCAO) surgery and reperfusion (MCAO/R) to establish a CIRI model. Neurological deficit score was evaluated using Garcia's scale. Cerebral infarction in rats was determined using TTC staining. Brain tissue morphology was assessed by HE staining. The expression of various proteins was measured using IF assay and western blot. EA or TG treatment could effectively ameliorate neurological disorders, attenuate cerebral infarction and reduce neuronal damage in brain tissue in CIRI rats. In addition, EA or TG treatment suppressed autophagy and pyroptosis in CIRI rats. More importantly, synergistic effects of EA and TG intervention in CIRI rats were observed in ameliorating neuronal damage and suppressing autophagy and pyroptosis, while Rapa, an inducer of autophagy, strengthened these effects in MCAO/R-induced rats. Furthermore. Rapa reversed EA in combination with TG-mediated improvement of neuronal damage and suppression of autophagy and pyroptosis in CIRI rats. Notably, the PI3K/AKT/mTOR pathway was inactivated in CIRI rats and EA combined with TG enhanced the activation of the PI3K/AKT/mTOR pathway. LY294002, an inhibitor of the PI3K/AKT/mTOR pathway, stimulated autophagy and pyroptosis in CIRI rats and reversed EA combined with TG-mediated suppression of autophagy and pyroptosis. EA combined with TG suppressed pyroptosis, which was dependent on inhibition of autophagy in CIRI rats through activation of the PI3K/AKT/mTOR signaling pathway.

Highly Sensitive LC-MS/MS Method for Determination of Dexamethasone in Rat Plasma and Brain Tissue: An Application to Pharmacokinetic Study in Rats.

A highly sensitive and rapid LC-MS/MS method was developed and validated for the quantification of dexamethasone in rat plasma and brain tissue. Protein precipitation method was used for sample preparation. The separation of dexamethasone and the IS (labetalol) was achieved on an Atlantis dC18 column using an isocratic mobile phase (10 mM ammonium formate and acetonitrile, 25/75, v/v) delivered at 0.7 mL/min flow-rate. Dexamethasone and the IS were eluted at 1.03 and 1.06 min, respectively. The MS/MS transitions monitored were m/z 393.100 → 373.100 (dexamethasone) and 329.100 → 91.100 (IS). Method validation was performed as per FDA guidelines and all parameters met the acceptance criteria. The assay was validated with a quantification range of 0.05-1046 ng/mL in both matrices. The intraday and interday precision for were in the range of 2.62-7.28 and 2.76%-6.98% and 2.24-6.85 and 2.97%-6.37%, in plasma and brain tissue, respectively. Dexamethasone was stable in a series of stability conditions in both matrices. Post-intravenous administration to rats, dexamethasone concentrations in plasma and brain tissue were quantifiable up to 24 and 10 h, respectively. Dexamethasone half-life was ~2.30 h. Dexamethasone exhibited low clearance and moderate volume of distribution in plasma but in brain tissue the clearance and volume of distribution were high.

Increased Expression of MST1 in Patients With Epilepsy and in a Rat Model of Epilepsy.

Mammalian sterile20-like kinase 1 (MST1), a serine/threonine kinase frequently expressed, has emerged as pivotal modulator of multiple physiological and pathological conditions such as cellular growth, programmed cell death, oxidative stress, neurodegeneration, inflammation, and synaptic plasticity in the central nervous system. Various neurological diseases are associated with the activation of MST1. Epilepsy is a severe neurological disorder characterized by abrupt abnormal electrical activity in the brain and recurring spontaneous seizures. The most common pathological discoveries in patients and animal models with epilepsy are neuronal death, inflammation, neurodegeneration, neurogenesis, and axonal regrowth. The purpose of this study was to assess the levels of MST1 in serum and cerebrospinal fluid (CSF) specimens obtained from individuals diagnosed with epilepsy. In addition, it aimed to explore the expression pattern of MST1 in brain tissues of epileptic rats. We used enzyme-linked immunosorbent assay to measure the levels of CSF and serum MST1 in 10 epilepsy patients and 9 control patients. After creation of epilepsy models with healthy male Sprague-Dawley rats using lithium and pilocarpine, the expression of MST1 in the temporal cortex and hippocampus was evaluated at different time points (6h, 24h, 3days, 7days, 14days, and 30days after seizures) using immunofluorescence, immunohistochemistry, and Western blotting. In patients with epilepsy, the levels of CSF-MST1 were elevated (593.90±16.28 vs. 560.40±19.42pg/mL, p<0.05) compared to the control group. Accordingly, the serum-MST1 levels were 583.40±19.70pg/mL in the epilepsy group and 555.70±20.14pg/mL in the control group, demonstrating a statistically significant distinction (p<0.05). Levels of MST1 in CSF and serum could be of diagnostic help. Neuronal apoptosis in temporal cortex and hippocampus of epileptic rats was detected using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. MST1 was expressed in the neuronal membrane and cytoplasm of the temporal cortex and hippocampus. The expression of MST1 increased after seizures, showing a relatively high level within 30days and reaching its highest point on the seventh day after status epilepticus. The findings of this study indicate that the increased expression of MST1 protein in patients with epilepsy and epileptic rats might play a role in the development of epilepsy.

Antioxidant Effects of Moringa oleifera Against Abamectin-Induced Oxidative Stress in the Brain and Erythrocytes of Rats.

The current study was conducted to explore the phytochemical composition and in vitro antioxidant activity of Moringa oleifera leaves aqueous extract (MOLE), as well as its in vivo modulatory effects on abamectin (ABM)-induced oxidative stress in rat erythrocytes and brain tissue. Following extraction, the total phenolic, flavonoid, condensed tannin and ortho-diphenolic contents of MOLE were determined. High-performance liquid chromatography (HPLC) analysis allowed the identification and the quantification of 12 bioactive compounds: gallic acid, chlorogenic acid, caffeic acid, vanillic acid, quercetin, ferulic acid, ascorbic acid, alizarin, hesperidin, neohesperidin, resveratrol, and naringin. In vitro study: the assessment of the antioxidant activity of MOLE on the 2,2-diphenyl-1-picrylhydrazyl radical DPPH and the 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radical cation (ABTS), its ferric reducing power and its antioxidant effect on the β-carotene bleaching indicated that MOLE exhibited potent antioxidant activity, with an IC50 of 0.125mg/mL against DPPH radical, and an IC50 of 0.06mg/mL against ABTS radical. It also demonstrated notable ferric-reducing ability, with an EC50 of 1.4mg/mL and a strong inhibition of β-carotene bleaching with an IC50 of 1.36mg/mL. In vivo study: Twenty rats were equally divided into four groups. The first group served as a control and received distilled water by gavage. The second group (negative control) received ABM in drinking water at a dose of 1mg/kg body weight. The third group received MOLE at a dose of 200mg/kg of body weight by gavage. The fourth group received a combination of ABM and MOLE in the same manner and doses as described, for 3weeks. Body weight, brain relative and absolute weights, and nitric oxide levels were not affected by ABM. However, ABM significantly inhibited acetylcholinesterase (AChE) activity (p<0.001), decreased the activities of antioxidant enzymes, specifically superoxide dismutase (SOD) and glutathione S-transferase (GST) in cerebral tissue, and catalase (CAT) in erythrocytes (p<0.001). ABM also decreased reduced glutathione (GSH) levels in both the brain (p<0.001) and erythrocytes (p<0.05). In addition, malondialdehyde (MDA) levels significantly increased in the brains of ABM-intoxicated rats (p<0.01) compared to the control group. These results were accompanied by histopathological changes, notably the remarkable vacuolization of neuropil in brain tissue. Supplementation with MOLE in ABM-treated rats significantly ameliorated brain AChE (p<0.05) and GST activities, decreased MDA content, and improved GSH levels in both brain and erythrocyte homogenates (p<0.01). MOLE also restored the histopathological alterations observed in the ABM group. Computational modeling revealed that some of the tested molecules, including some present in the studied extract, bound human peroxiredoxin 5, CAT, and glutathione peroxidase with acceptable affinities, which, together with the established molecular interactions and tight embedding satisfactory support the in vivo results. Thus, it may be concluded that ABM impairs brain and erythrocyte function through oxidative damage, and these effects could be prevented by MOLE, likely due to its antioxidant activity.

NOD-like receptor X1 promotes autophagy and inactivates NLR family pyrin domain containing 3 inflammasome signaling by binding autophagy-related gene 5 to alleviate cerebral ischemia/reperfusion-induced neuronal injury.

Ischemic strokes pose serious risks to human health. We aimed to elucidate the function of NOD-like receptor X1 (NLRX1) in a rat middle cerebral artery occlusion (MCAO)-induced cerebral ischemia/reperfusion injury (CIRI) model and in an oxygen-glucose deprivation/reperfusion (OGD/R)-treated human microglial cell line (HMC3) model. Following NLRX1 upregulation, infarct volumes were measured with 2,3,5-triphenyltetrazolium chloride staining and pathological examination was conducted with hematoxylin-eosin staining. Results suggested that levels of NLRX1 were decreased in brain tissue of MCAO rats and in OGD/R-stimulated HMC3 cells. NOD-like receptor X1 overexpression mitigated the neuronal damage, reduced tumor necrosis factor-α and interleukin-6 expression, alleviated microglial activation, and induced autophagy in vivo and in vitro. Additionally, a coimmunoprecipitation assay indicated that NLRX1 bound to autophagy-related gene 5 (ATG5) to elevate ATG5 expression in HMC3 cells. Further, the elevated NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD, and cleaved caspase 1 expression in MCAO rats and HMC3 cells with OGD/R induction was reduced after NLRX1 upregulation. Importantly, ATG5 depletion abrogated the effects of NLRX1 elevation on NLRP3 inflammasome signaling. These results indicate that NLRX1 promotes autophagy and inactivates NLRP3 inflammasome signaling by binding ATG5 in experimental cerebral ischemia. These data may help the development of novel therapeutic strategies for ischemic stroke.

Experimental Measurement and Mathematical Quantification of Fixed-Charged Density in Rat and Pig Brain Tissue.

Cerebral edema is associated with poor prognosis because brain swelling within the rigid skull raises intracranial pressure, exacerbating secondary injuries following traumatic brain injury. Brain swelling can be characterized by triphasic biomechanics, which models brain tissue as a mixture of a deformable porous solid matrix with a negative fixed-charged density (FCD), water, and monovalent counterions. When brain cells die, the intracellular FCD is exposed, attracting cations into the cells. The increase in intracellular solute concentration generates osmotic pressure via the Gibbs-Donnan effect, driving water into cells and causing swelling. This study quantifies the FCD of rat and pig brain tissue by measuring the pressure generated by tissue within a confined volume as cells died. Rat brain tissue generated an averaged swelling pressure of 52.92 ± 20.40mmHg (mean ± one standard deviation). Variations were observed between pig cortical white matter (7.14 ± 4.79mmHg) and cortical gray matter (33.86 ± 11.89mmHg). The corresponding FCD values were 42.54 ± 8.14mEq/L for rat brain tissue, and 15.18 ± 5.38mEq/L and 34.22 ± 6.31mEq/L for pig cortical white and gray matter, respectively. Treating the rat brain tissue with DNAse, heparinase I, heparinase III, and chondroitinase ABC to degrade FCD significantly reduced swelling pressure. Good agreement between the experimental and numerically simulated responses supported the role of the FCD in cerebral edema formation. The reported FCD values can improve the biofidelity of computational models to predict post-traumatic cerebral edema, aiding the improvement of safety systems.

Antioxidant Properties of Resveratrol in the Brain Tissues of Rats after Radiotherapy

Background: In recent years, there has been growing interest in the use of herbal products as complementary or alternative therapies for cancer patients. RVT has been extensively studied for its potential role in managing oxidative stress in cancer patients undergoing treatment. Method: In this study, the radioprotective effects of Resveratrol (RVT) (200 mg/kg) were evaluated in the brain tissues of rats after Radiation Therapy (RT). 20 male adult Wistar rats weighing 180–200 g were used. The animals were exposed to single-fraction Irradiation (IR) (15 Gy) using a linear accelerator unit (Siemens Primus) at a dosage rate of 200 cGy/min at a distance of 100 cm from the source to the axis. Results: The results of the study showed that compared to the IR group, administration of RVT decreased the levels of MDA and NOx, and increased the levels of CAT and SOD significantly (p&lt;0.05). Conclusion: Finally, our finding suggests that RVT could have radioprotective effects on the brain by enhancing antioxidant defense mechanisms.

LCN2 Regulates Microglia Polarization Through the p38MAPK-PGC-1α-PPARγ Pathway to Alleviate Traumatic Brain Injury.

Traumatic brain injury (TBI) is a common traumatic event that imposes a significant burden on families and society. Lipocalin (LCN) is a class of multifunctional secreted lipoprotein molecules. This study aimed to explore the role and possible mechanism of LCN2 in TBI. A rat model of TBI was constructed and adeno-associated virus-coated shRNA-LCN2 was used to silence LCN2 expression. The modified neurological severity score (mNSS), learning and memory ability, pathological injury of brain tissue, number of neurons, and expression of neurotrophic factors were analyzed, and the expression of inflammatory factors, M1/M2 polarization of microglia, and p38MAPK-PGC-1α-PPARγ pathway after LCN2 silencing were further detected. Results found that LCN2 was highly expressed in the brain tissue of TBI rats, and there were obvious learning and cognitive impairments and pathological injury of brain tissue. After silencing LCN2, the mNSS was further increased, and the learning and cognitive ability was weakened. Similarly, silencing LCN2 increased the brain tissue water content, aggravated the histopathology degree, decreased the number of surviving neurons, and reduced the expression of neurotrophic factors in TBI model rats. In addition, the expression of M1 proinflammatory cytokines and polarization markers in microglia of TBI was increased, and the expression of M2 cytokines and markers was decreased after silencing LCN2. Silencing LCN2 also inhibited the activation of the p38MAPK-PGC-1α-PPARγ pathway. In conclusion, LCN2 was released by surviving neurons after TBI, and the increased LCN2 activated the p38MAPK-PGC-1α-PPARγ pathway, which promoted M2 polarization of microglia, and secreted neurotrophic factors, thereby alleviating secondary brain injury.

Predicting Protein Pathways Associated to Tumor Heterogeneity by Correlating Spatial Lipidomics and Proteomics: The Dry Proteomic Concept.

Prediction of proteins and associated biological pathways from lipid analyses via matrix-assisted laser desorption/ionization (MALDI) MSI is a pressing challenge. We introduced "dry proteomics," using MALDI MSI to validate spatial localization of identified optimal clusters in lipid imaging. Consistent cluster appearance across omics images suggests association with specific lipid and protein in distinct biological pathways, forming the basis of dry proteomics. The methodology was refined using rat brain tissue as a model, then applied to human glioblastoma, a highly heterogeneous cancer. Sequential tissue sections underwent omics MALDI MSI and unsupervised clustering. Spatial omics analysis facilitated lipid and protein characterization, leading to a predictive model identifying clusters in any tissue based on unique lipid signatures and predicting associated protein pathways. Application to rat brain slices revealed diverse tissue subpopulations, including successfully predicted cerebellum areas. Similarly, the methodology was applied to a dataset from a cohort of 50 glioblastoma patients, reused from a previous study. However, among the 50 patients, only 13 lipid signatures from MALDI MSI data were available, allowing for the identification of lipid-protein associations that correlated with patient prognosis. For cases lacking lipid imaging data, a classification model based on protein data was developed from dry proteomic results to effectively categorize the remaining cohort.

Effect of vitamin D and omega-3 on the expression of endoplasmic reticulum-associated protein degradation and autophagic proteins in rat brain

Abstract Objectives Valosin-containing protein (p97/VCP) and its cofactor, small p97/VCP-interacting protein (SVIP), are involved in the endoplasmic reticulum-associated degradation pathway (ERAD). We investigated the cellular localization of vitamin D receptor (VDR), ERAD, and autophagic proteins (LC3B and p62) in rat brain tissue. Methods There were four groups consisting of 24 Wistar albino rats: control and treatment groups for vitamin D, omega-3, and both vitamin D and omega-3. Brain tissues were stained with hematoxylin-eosin, azan trichrome, and toluidine blue for histopathological evaluation. The immunohistochemistry assay was performed for VDR, p97/VCP, SVIP, LC3B, and p62 in rat brain sections. Results The immunoexpression of VDR and p97/VCP was significantly increased in hippocampus and cortex of brain tissue from the vitamin D-supplemented group. Furthermore, the protein expression level of SVIP reached the highest level in vitamin D-treated group. LC3B and p62 revealed reduced expressions in vitamin D-treated group in rat brain and hippocampus, in contrast to p97/VCP, SVIP, and VDR. Conclusions Vitamin D and omega-3 supplementations had no negative effects at a cellular level on hippocampus and cortex of the brain tissue. Vitamin D increased the expression of the proteins that are related to the ERAD pathway, whereas it reduced the expression of the proteins in the autophagy pathway. Also, in this study, SVIP expressions were shown in rat hippocampus and cortex of the brain tissue.

Therapeutic potency of kaempferol against Naja haje venom induced neurotoxicity, inflammation, biological activities, and antioxidant system damage: a pre-clinical antivenom evaluation.

Naja haje envenoming manifests organ system disorders leading to severe fatalities due to the venom's toxins. The neutralizing capacity of kaempferol has been reported against some medically significant snake venoms with exception of N. haje venom (NhV). This current study assessed the neutralizing profile of kaempferol against toxicities induced by NhV using in vitro and in vivo methods. In in vitro, NhV induced wide spectrum of toxic biological activities with substantial increase in hemorrhagic, anticoagulating, and hemolytic effects. Likewise in the in vivo study, the venom caused hematological disorders by inducing acute anemia, thrombocytopenia, and leucopenia in envenomed rats. Also, the venom caused detrimental effect on the antioxidant defense system of the brain through significant (P < 0.05) elevation of malondialdehyde (MDA), nitrite (NIT), and suppression of reduce glutathione (GSH) antioxidant, superoxide dismutase (SOD), catalase (CAT), and glutathione transferase (GST) enzymes. Additionally, the levels of neurotoxicity biomarkers, monoamine oxidase (MAO) and acetylcholinesterase (AChE), and pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), were significantly (P < 0.0.5) enhanced by NhV in the brain of envenomed rats. Severe pathohistological effects were observed in brain tissues of the envenomed rats. However, kaempferol substantially (P < 0.05) inhibited the NhV-induced biological activities, normalized the hematological disorders, enhanced antioxidants system functions, and significantly (P < 0.05) suppressed the levels of neurotoxicity biomarkers and pro-inflammatory cytokines. Severe structural alterations observed in the brain tissues were ameliorated after kaempferol treatment. Further exploration of kaempferol could lead to the development of an alternative therapy for treatment of N. haje envenoming.

Nitrogen-rich porous polymer as a solid-phase microextraction coating for the ultrasensitive analysis of nicotine and its metabolites in different rat brain regions

Nicotine, a major component of tobacco smoke, exerts complex effects on the brain, including dependence and potential neurotoxicity. Understanding its distribution and metabolism in different brain regions is crucial for elucidating its neurological impact. This study presents a new solid-phase microextraction (SPME) method using a nitrogen-rich porous polymer coating (BDTB-MBD) that simultaneously quantified nicotine and its six metabolites in different rat brain regions. The coating material exhibited excellent stability with a high surface area (1001.7 m2/g), suitable pore diameter (5.28 nm), and excellent hydrophilic and hydrophobic properties. Under optimal conditions, the SPME tandem ultra-high-performance liquid chromatography-triple quadrupole mass spectrometry (UHPLC-MS/MS) method exhibited a wide linear range (0.01–100 μg L−1), low limits of detection ranging from 0.002–0.020 μg L−1, limits of quantifications ranging from 0.006–0.070 μg L−1, and satisfactory repeatability and reproducibility. The spiked recovery rates ranged from 77.1 % to 99.6 %, indicating that the established method was sensitive, accurate, and reliable. Density functional theory calculations revealed strong non-covalent interactions between BDTB-MBD and analytes, providing insights into the adsorption mechanism. The SPME-UPLC-MS/MS method successfully tracked the pharmacokinetics of nicotine in different rat brain tissues following intraperitoneal injection. The results demonstrated rapid absorption with a regional distribution of nicotine, followed by its gradual metabolism into cotinine, nornicotine, and other metabolites. Notably, the concentration profiles varied across brain regions, highlighting the importance of considering regional specificity in nicotine brain research. Compared with traditional techniques such as solid phase extraction, this approach offers a valuable tool for studying nicotine distribution and metabolism in the brain, with potential applications in neuroscience and drug monitoring.

Protective effects of puerarin combined with bone marrow mesenchymal stem cells on nerve injury in rats with ischemic stroke

ABSTRACT Background Bone marrow mesenchymal stem cells (BM-MSCs) transplantation shows promise for treating ischemic stroke, but the ischemic environment that follows cerebral infarction hinders the survival of transplanted cells. We aimed to study the effects of puerarin (Pue) in combination with BM-MSCs on cerebral ischemic injury. Methods After middle cerebral artery occlusion (MCAO) models were prepared by suture-occluded method, rats were randomly allocated to the sham, MCAO, Pue (50 mg/kg), BM-MSCs (2×106), and BM-MSCs+Pue groups. The neurological function, infarct area, levels of inflammation-related factors, brain tissue damage, apoptosis, BrdU, Beclin1, and LC3 levels were then assessed. Results Pue and BM-MSCs reduced the modified neurological severity score, cerebral infarction area, and serum inflammation-related factor levels for MCAO rats. Furthermore, Pue and BM-MSCs interventions ameliorated brain tissue damage, and repressed apoptosis of brain tissues in MCAO rats. Moreover, Pue or BM-MSCs enhanced BrdU expression, restrained LC3II/LC3I ratio and Beclin 1 expression in MCAO rats’ brain tissues. Importantly, the combination of Pue and BM-MSCs exhibited more pronounced effects on aforementioned outcomes. Conclusion The combination of Pue and BM-MSCs facilitated the recovery of neurological function in rats after cerebral ischemic damage, and the mechanisms may correlate with the repression of neuronal apoptosis, inflammation, and autophagy.

Correlation analysis of LXR and its target genes COX2 and CETP with the severity of OSAHS in obese young rats.

To analyse the relationships between the expression levels of liver X receptor (LXR), cyclooxygenase-2(COX2) and cholesterol ester transfer protein (CETP) and the severity of obstructive sleep apnoea hypopnoea syndrome (OSAHS) in obese young rats, to obtain information for basic research on OSAHS in obese children. Twenty-four 3-4-week-old young rats were randomly assigned to the normal control group, obesity group, OSAHS group, obesity and OSAHS group. We used polysomnography to measure the obstructive apnoea hypopnoea index (OAHI) to assess the severity of OSAHS and western blotting to test the expression levels of LXRα, COX2, and CETP in the liver, heart, kidney, and brain tissues. LXR, COX2, and CETP expression levels in the remaining groups were considerably higher than those in the control group (P < 0.05). Compared with those in the obesity group, LXRα, COX2, and CETP expression levels in the obesity and OSAHS group were considerably greater in the liver, kidney, and heart tissues (P < 0.05); the brain tissues of the obesity and OSAHS group showed considerably higher expression levels of COX2 and CETP (P < 0.05). Compared with those in the OSAHS group, LXRα, COX2, and CETP expression levels in the obesity and OSAHS group were significantly greater in all tissues (P < 0.05). The expression levels of LXRα, COX2, and CETP and obesity increased with increasing OSAHS severity (r = 0.777, P < 0.01; r = 0.728, P < 0.01; r = 0.793, P < 0.01; r = 0.786, P < 0.01; and r = 0.698, P < 0.01), and the oxygen concentration increased with decreasing OSAHS severity(r=-0.576, P < 0.01). LXR, COX2, and CETP expression levels were significantly increased in the liver, kidney, heart, and brain tissues of young rats with obesity and OSAHS, and were positively correlated with the severity of OSAHS.

Imaging Mass Spectrometry of Sulfatide Isomers from Rat Brain Tissue Using Gas-Phase Charge Inversion Ion/Ion Reactions.

Sulfatides are abundant components of the brain, and dysregulation of these molecules has been linked to several diseases. In sulfatide structures, a sugar is linked to a sphingoid backbone via an α-glycosidic or β-glycosidic linkage. While sulfatides are readily generated in negative ion mode imaging mass spectrometry experiments, resolving sulfatide diastereomers is challenging; therefore, identifications are usually reported as a single sulfatide. Herein, a gas-phase charge inversion ion/ion reaction between sulfatides and a strontium tris-phenanthroline [Sr(Phen)3]2+ reagent is performed to separate the diastereomers, as they form complexes containing different numbers of phenanthroline ligands. The ability to separate these diastereomers using the reaction alone, without the need for any further dissociation, allows for the workflow to be readily implemented in an imaging mass spectrometry experiment. Imaging mass spectrometry was performed on sulfatides generated directly from rat brain tissue, and both the α- and β-linked sulfatide images were obtained.

Система метаболізму серотоніну в головному мозку щурів за умов розвитку глутаматіндукованого ожиріння та його корекції нанокристалічним діоксидом церію

One of the causes of obesity is the body’s energy imbalance. The aim of our work was to investigate the serotonin system in the brain tissue of rats with glutamate-induced obesity and its correction with nanocrystalline cerium dioxide. The research was conducted on 30 white rats, divided into 3 groups of 10 animals each: 1st − intact control, 2nd − simulation of obesity by administration of monosodium glutamate to neonatal animals, 3rd − correction of obesity using nanocrystalline cerium dioxide against the background of neonatal administration of monosodium glutamate. To confirm the presence of obesity, at 4 months of age, rats were weighed, naso-anal length was measured, and Lee’s index was calculated. It was found that rats after neonatal administration of monosodium glutamate developed obesity, and the content of serotonin in the brain decreased by 72.9% compared to the control. The content of tryptophan, a precursor in the synthesis of serotonin, in rats with glutamate-induced obesity was 93.3% lower compared to controls. Tryptophan hydroxylase activity in the brain of rats with glutamate-induced obesity tended to decrease, and tryptophan decarboxylase activity increased by 65.9% compared to the controls. The activity of monoamine oxidase in the brain of rats after neonatal administration of monosodium glutamate increased by 41.7% compared to the control, which indicates enhanced degradation of serotonin. Indoleamine-2,3-dehydrogenase activity in the brain of rats with glutamate-induced obesity increased by 122.2%, this evidences activation of the alternative kynurenine pathway of tryptophan metabolism in the brain. This may also be one of the reasons for the reduced serotonin content in the brains of rats with glutamate-induced obesity. Periodic administration of nanocrystalline cerium dioxide to rats after neonatal sodium glutamate administration prevented obesity and led to an increase in serotonin and tryptophan content in the brain by 171.6% and 72.7%, respectively, a decrease in tryptophan decarboxylase activity by 15.1%, an increase in monoamine oxidase activity by 60.7% and a decrease in indoleamine2,3-dihydrogenase activity by 17.7% compared to rats after neonatal sodium glutamate administration. We conclude that the serotonin system is involved in the development of glutamate-induced obesity, and that periodic administration of nanocrystalline cerium dioxide significantly improves serotonin metabolism parameters.

NEFL Modulates NRN1-Mediated Mitochondrial Pathway to Promote Diacetylmorphine-Induced Neuronal Apoptosis.

Diacetylmorphine abuse is a major social problem that jeopardizes the world, and abuse can cause serious neurological disorders. Apoptosis plays an important role in neurological diseases. A previous study by our group found that the brain tissue of diacetylmorphine-addicted rats showed severe vacuole-like degeneration and increased apoptosis, but the exact mechanism has not yet been reported. We used TMT technology to sequence the diseased brain tissue of rats, and selected neurofilament light chain (NEFL) and neuritin (NRN1) as the focus of our research. We explore the possible roles and mechanisms played by both. Based on the construction of apoptotic cell model, we used overexpression/silencing lentiviral vectors to interfere with the expression of NEFL in PC12 cells, and the results suggested that NEFL could regulate NRN1 to affect the apoptosis level. To further understand the specific mechanism, we used transmission electron microscopy to observe the ultrastructure of apoptotic cells, and the results showed that compared with the control group, mitochondria in the model group showed obvious vacuolation as well as expansion, a significant increase in the accumulation of ROS, and a significant decrease in the mitochondrial membrane potential; after overexpression/silencing of NEFL, these changes were found to occur along with the alteration of NEFL expression. In summary, we conclude that diacetylmorphine induces neuronal apoptosis, and the specific mechanism is that NEFL regulates the NRN1-mediated mitochondrial pathway to promote apoptosis.

Flaxseed Oil: Safeguarding Neurological Health through Apoptosis and Oxidative Damage Defense

: The present study aims to investigate the neuroprotective properties of flaxseed oil (FSO) in reducing cadmium-induced neurotoxicity. The neuroprotective properties of FSO were observed in rats by examining the expression of caspase-3 and Bcl-2 to determine the antiapoptotic capabilities of FSO. Methods: Rats were given cadmium orally at a dosage of 5 mg/kg/day for 30 days, along with flaxseed oil (FSO) at doses of 2ml/kg/day and 3ml/kg/day for the same duration. The Morris watermaze test (MWM) and the Novel object recognition test (NOR) were performed to evaluate learning and memory abilities. We quantified the amounts of glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), and acetylcholinesterase inhibitory activity (AChE) in the entire brain homogenate. Additionally, apoptosis and histopathology studies were conducted on rat brain tissues. Results: Intoxication with cadmium was associated with significant impairment of learning and memory in Morris watermaze (MWM) and novel object recognition (NOR) tests. The group that consumed Cd showed elevated levels of MDA, NO, and AChE in the brain homogenate, higher levels of caspase-3 and Bcl-2, and decreased levels of GSH compared to the control group. Animals treated with FSO exhibited improved learning and memory function, along with balanced levels of oxidative and cholinergic activity in brain tissue. Additionally, levels of caspase-3 and Bcl-2 were reduced in a similar way to the control group. Conclusions: The study demonstrates that flaxseed oil has positive effects by raising GSH and antiapoptotic potential levels while reducing MDA, NO, and AChE levels in the brain. This contributes to neuroprotection and decreases neuronal death, as supported by histopathological findings.

Assessment of the Potential Toxic Consequences of Energy Drinks on the Brain Tissue of Maternal Wister Rats Throughout Gestation and Lactation

Assessment of the Potential Toxic Consequences of Energy Drinks on the Brain Tissue of Maternal Wister Rats Throughout Gestation and Lactation