Glial Fibrillary Acidic Protein Expression Research Articles

Secretome from hypoxic mesenchymal stem cells as a potential therapy for ischemic stroke: Investigations on VEGF and GFAP expression

Ischemic stroke is a sudden onset of neurological deficit resulting from a blockage in cerebral blood vessels, which can lead to brain tissue damage, chronic disability, and increased risk of mortality. Secretome from hypoxic mesenchymal stem cells (SH-MSC) is a potential therapy to improve neurological deficit by increasing the expression of vascular endothelial growth factor (VEGF) and reducing glial fibrillary acidic protein (GFAP). These effects can reduce the infarction area of ischemic stroke. Therefore, the aim of this study was to analyze the effect of 150 μL and 300 μL SH-MSC injection on VEGF and GFAP expression as well as the improvement of infarction area in ischemic stroke animal model. A post-test-only experimental design with consecutive sampling was used, with Rattus norvegicus as subjects. Stromal mesenchymal stem cells (S-MSCs) were isolated from the umbilical cords of rats at 21 days of gestation. Secretome production by the S-MSCs was induced under a hypoxic condition, and subsequently isolated. The resultant secretome was administered to rats subjected to middle cerebral artery occlusion (MCAO) at doses of 150 μL (P1 group) and 300 μL (P2 group). The results showed that the infarction area was reduced in P1 (p<0.001) and P2 groups (p<0.001). SH-MSC at a dose of 300 μL increased the expression of VEGF (p=0.028) and reduced the expression of GFAP (p=0.001). In conclusion, secretome from hypoxic S-MSC could potentially improve ischemic stroke by upregulating VEGF expression and downregulating GFAP expression.

Hepatoprotective and neuroprotective effects of quinacrine against bile duct ligation-induced hepatic encephalopathy in rats: Role of bone morphogenetic proteins signaling

AimsThis study aimed to assess the potential protective effect of quinacrine, an FDA approved antimalarial drug with reported anti-inflammatory effects, on hepatic encephalopathy (HE) in a bile duct ligation (BDL) experimental model and to investigate the mechanisms responsible for this effect, namely those associated with the liver-brain axis, particularly, bone morphogenetic protein 2 (BMP2) signaling. Materials and methodsFive groups of rats were selected at random: sham, BDL, (BDL+ quinacrine 5), (BDL+ quinacrine 10), and (quinacrine 10 + sham). Daily Intraperitoneal (I.P.) administration of quinacrine was initiated on the surgery day and continued for 28 days. Key findingsResults showed that rats that underwent BDL exhibited marked elevation of serum liver enzymes, ammonia, total bilirubin, together with oxidative stress, inflammation, dysregulated farnesoid x receptor (FXR), dysregulated BMP2 signaling and escalated fibrotic markers indicating hepatotoxicity, cholestasis and fibrosis. Besides, neurotoxicity was detected as manifested by cognitive deficits and dysregulation of hippocampal FXR, BMP2 signaling, WNT3A signaling, brain derived neurotrophic factor (BDNF), phospholipase A2 (PLA2) and glial fibrillary acidic protein (GFAP). In contrast, co-treatment with quinacrine mitigated BDL-induced hepatotoxicity, cholestasis, fibrosis, and neurotoxicity. Notably, quinacrine improved learning and memory and restored FXR, BMP2 signaling in the liver and hippocampus. In addition, quinacrine restored hippocampal WNT3A signaling, BDNF, whereas it downregulated expression of hippocampal PLA2 and GFAP. SignificanceThese findings demonstrated implication of BMP2 signaling in the molecular process of BDL-induced HE and proposed that quinacrine has potential hepatoprotective and neuroprotective properties against HE.

GW117 induces anxiolytic effects by improving hippocampal functions

GW117 functions as both an MT1/MT2 receptor agonist and a 5-HT2C receptor antagonist. This study aimed to investigate the anxiolytic effects of GW117 through behavioral assessments, including the open field test and novelty-suppressed feeding test (NSFT) within a chronic unpredictable mild stress (CUMS) model. GW117 was administered via oral gavage for 21 days to evaluate its sustained anxiolytic effects, with behavioral tests including the NSFT, the Vogel-conflict test, and the O-maze test. To explore the underlying mechanisms, we performed Western blot analyses to assess the expression levels of BCL2-Associated X (Bax), cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), brain-derived neurotrophic factor (BDNF), and glial fibrillary acidic protein (GFAP). Additionally, BrdU labeling and immunofluorescence staining were used to examine changes in neuronal regeneration and astrocytogenesis. Our results demonstrated that GW117 produced significant anxiolytic effects across all behavioral assays, both in the CUMS model and during long-term administration. Mechanistic studies revealed that GW117 notably increased the expression of BDNF, GFAP, and Bcl-2, while reducing Bax and cleaved caspase-3 levels in the hippocampus of CUMS model rats. Furthermore, the populations of BrdU-positive and GFAP-positive cells were elevated. These findings suggest that GW117 exerts anxiolytic effects, potentially through enhancements in hippocampal function.

Ginsenoside Rb1 ameliorates hippocampal neuroinflammation in rats after intracerebral hemorrhage by inactivating the TLR4/NF-kB pathway.

This work elucidated the therapeutic effect and mechanism of ginsenoside Rb1 on intracerebral hemorrhage (ICH). ICH rat models were treated by ginsenoside Rb1. Modified neurological deficit score, and Y-maze and Morris water-maze tests were performed on rats. Hippocampal neuronal damage was observed by Nissl staining. Rat primary astrocytes were exposed to ginsenoside Rb1, Hemin, and lipopolysaccharide (LPS). TNF-α, IL-1β, and IL-6 levels were assessed via enzyme-linked immunosorbent assay. TLR4/NF-kB pathway activity was appraised by Western blot. Immunofluorescence staining was for hippocampal glial fibrillary acidic protein (GFAP) expression and P65 protein location in hippocampus and astrocytes. In rats after ICH, ginsenoside Rb1 ameliorated neurological impairment and hippocampal neuronal damage; improved learning and memory ability; reduced brain water content; decreasedhippocampal TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and declined hippocampal GFAP expression. In rat primary astrocytes exposed to Hemin, ginsenoside Rb1 declined TNF-α, IL-1β, and IL-6; inactivated TLR4/NF-kB pathway; and hindered P65 protein entry into nucleus. However, these functions of ginsenoside Rb1 on the Hemin-induced astrocytes were abolished by LPS. Ginsenoside Rb1 has promising future for clinical ICH treatment, which exerts therapeutic effect on ICH by ameliorating hippocampal neuroinflammation via inactivating the TLR4/NF-kB pathway.

Immunohistochemical Expression of GFAP in the Brain Astrocytes of Deceased Newborns Depending on the Postmortem Interval.

The changes in astrocytes and their role in the development of brain diseases can be identified by morphological analysis of tissue specimens, in particular, by immunohistochemical detection of glial fibrillary acidic protein (GFAP). The study presents analysis of GFAP expression in white matter astrocytes of deceased newborns depending on the duration of the postmortem period. Autopsy material of the brain tissue obtained from 48 deceased newborns was divided into 8 groups depending on the duration of the postmortem period. Immunohistochemical analysis was performed with antibodies to GFAP in tissue samples taken from the superior and inferior brain areas relative to the position of the body stored before autopsy. The area of GFAP+ staining per field of view was determined in the white matter using an image analysis system. Morphometric analysis revealed a decrease in the mean values of the area of GFAP+ staining, i.e. the number of fibrotic astrocytes and their processes decreased with increasing the duration of the postmortem period. The mean areas of GFAP+ staining in the superior and inferior areas of the white matter did not differ significantly between the groups. The identified changes reflect the development of nonspecific postmortem changes which should be considered when taking tissue samples for molecular biological studies and in differential forensic diagnosis with lifetime lesions and diseases.

Salidroside ameliorates cerebral ischemic injury and regulates the glutamate metabolism pathway in astrocytes.

Salidroside (SA) is the main active component of Rhodiola rosea L., with potential in treating cardiovascular and cerebrovascular diseases and cerebral ischemia. However, its efficacy and mechanism in cerebral ischemia remain unclear, particularly regarding its effect on glutamate (Glu) metabolism. In this paper, we aimed to investigate the efficacy of SA in treating cerebral ischemia and its pharmacological mechanism. We studied the effects of SA on SD rats with cerebral ischemia, evaluating neurobehavior, cerebral water content, infarct size, and brain microstructure. We also assessed its impact on glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), and glutamate transporter 1 (GLT-1) proteins using immunohistochemistry and Western blot. Additionally, we used SVGp12 cells to simulate cerebral ischemia and measured Glu levels and used Western blot to observe the level of GS and GLT-1. SA improved neural function, reduced infarct size, and regulated GSH and Glu levels in rats. In cell experiments, SA increased cell viability and decreased Glu concentration after ischemia induction. It also regulated the expression of GFAP, GS, and GLT-1. SA alleviates cerebral ischemia-induced injury by acting on astrocytes, possibly through regulating the glutamate metabolic pathway.

Honey Enriched with Additives Alleviates Behavioral, Oxidative Stress, and Brain Alterations Induced by Heavy Metals and Imidacloprid in Zebrafish.

Environmental concerns have consistently been a focal point for the scientific community. Pollution is a critical ecological issue that poses significant threats to human health and agricultural production. Contamination with heavy metals and pesticides is a considerable concern, a threat to the environment, and warrants special attention. In this study, we investigated the significant issues arising from sub-chronic exposure to imidacloprid (IMI), mercury (Hg), and cadmium (Cd), either alone or in combination, using zebrafish (Danio rerio) as an animal model. Additionally, we assessed the potential protective effects of polyfloral honey enriched with natural ingredients, also called honey formulation (HF), against the combined sub-chronic toxic effects of the three contaminants. The effects of IMI (0.5 mg·L-1), Hg (15 μg·L-1), and Cd (5 μg·L-1), both individually and in combination with HF (500 mg·L-1), on zebrafish were evaluated by quantifying acetylcholinesterase (AChE) activity, lipid peroxidation (MDA), various antioxidant enzyme activities like superoxide dismutase and glutathione peroxidase (SOD and GPx), 2D locomotor activity, social behavior, histological and immunohistochemical factors, and changes in body element concentrations. Our findings revealed that all concentrations of pollutants may disrupt social behavior, diminish swimming performances (measured by total distance traveled, inactivity, and swimming speed), and elevate oxidative stress (OS) biomarkers of SOD, GPx, and MDA in zebrafish over the 21-day administration period. Fish exposed to IMI and Hg + Cd + IMI displayed severe lesions and increased GFAP (Glial fibrillary acidic protein) and S100B (S100 calcium-binding protein B) protein expression in the optic tectum and cerebellum, conclusively indicating astrocyte activation and neurotoxic effects. Furthermore, PCNA (Proliferating cell nuclear antigen) staining revealed reduced cell proliferation in the IMI-exposed group, contrasting with intensified proliferation in the Hg + Cd group. The nervous system exhibited significant damage across all studied concentrations, confirming the observed behavioral changes. Moreover, HF supplementation significantly mitigated the toxicity induced by contaminants and reduced OS. Therefore, the exposure to chemical mixtures offers a more complete picture of adverse impacts on aquatic ecosystems and the supplementation with bioactive compounds can help to reduce the toxicity induced by exposure to environmental pollutants.

Molecular Mechanisms of GFAP and PTPRC in Alzheimer's Disease: An Analysis of Neuroinflammatory Response and Progression.

Alzheimer's disease (AD) is a complex neurological disorder that progressively worsens. Although its exact causes are not fully understood, new research indicates that genes related to non-neuronal cells change significantly with age, playing key roles in AD's pathology. This study focuses on a protein network centered on Glial Fibrillary Acidic Protein (GFAP) and Protein Tyrosine Phosphatase Receptor Type C (PTPRC). The Key Findings of this Study Include: 1. A significant correlation was observed between GFAP and PTPRC expression throughout AD progression, which links closely with clinical phenotypes and suggests their role in AD pathology. 2. A molecular network centered on GFAP and PTPRC, including Catenin Beta 1 (CTNNB1) and Integrin Beta 2 (ITGB2), showed distinct changes in interactions, highlighting its regulatory role in AD. 3. Analysis of GSE5281 data revealed a decline in the interaction strength within this network, pointing to potential desynchronization as a biomarker for AD. 4. SVM diagnostic models comparing GFAP expression and coupling values confirmed this desynchronization, suggesting it worsens with AD progression. Based on these findings, it is hypothesized that as AD progresses, the GFAP- and PTPRCcentered molecular framework undergoes significant changes affecting key biological pathways. These changes disrupt immune regulation and cellular functions, increasing immune cell activation and inflammation in the brain. This may impair neuronal communication and synaptic functionality, exacerbating AD's pathology. To verify these findings, Support Vector Machine (SVM) diagnostic models and correlation analyses were used to examine changes in this network, indicating that its dysregulation significantly affects AD progression.

Bihemispheric IDH-Wildtype Glioblastoma with Unilateral FGFR3-TACC3 Fusion in Patient with Breast Cancer History: A Case Report and Literature Review

Abstract Introduction/Objective Adult IDH-wild type glioblastomas comprise a heterogeneous spectrum of neoplasms, characterized by poor prognosis and resistance to the chemoradiotherapy. For WHO integrated diagnosis classification and to establish treatment options, molecular analysis is necessary. Herein, we present a case of a glioblastoma, IDH-wildtype with involvement of both cerebral hemispheres and an uncharacteristic in-frame fusion limited to one hemisphere. Methods/Case Report The patient is a 52-year-old woman with past medical history of metastatic breast cancer who presented with headache and worsening facial pain. Brain magnetic resonance imaging brain demonstrated a right frontal lobe lesion with vasogenic edema. The patient was treated with Gamma Knife radiosurgery. Scans revealed enlargement and a new left frontal lobe lesion. Bihemispheric tumor resection and GammaTile placement was undertaken. Results (if a Case Study enter NA) Histologically, the tumor was composed of hypercellular astrocytes, microvascular proliferation, and necrosis with no evidence of metastatic disease. Immunohistochemistically, neoplastic cells showed glial fibrillary acidic protein expression and elevated Ki-67 proliferation index. Molecular examination revealed in the right hemisphere lesion post-radiation (1) FGFR3::TACC3 (exon 17::exon 11) fusion and (2) TERT promoter, while the left hemisphere lesion which did not receive radiation showed clinically relevant variants in (1) TERT promoter, (2) TP53, (3) NF1, and (3) PIK3CA without identification of a fusion. An integrated diagnosis of glioblastoma, IDH- wildtype, CNS WHO grade 4 was established bilaterally. Conclusion The fibroblast growth factor receptor 3 (FGFR3)-transforming acidic coiled-coil 3 (TACC3) fusion is identified as a rare molecular feature in glioblastomas with an estimated prevalence of 4%. Clinical trials suggest that F3T3-positive tumors have a better prognosis than those without the translocation. The identification of the oncogenic FGFR3-TACC3 fusion highlights the possibility of identifying patients potentially responsive to targeted therapy with FGFR kinase inhibitors. The significance of the molecular differences in the right and left hemisphere lesions is uncertain; glioblastomas are heterogeneous tumors with intra-and intertumoral heterogeneity but it may suggest independent origins.

Semaglutide ameliorates Alzheimer's disease and restores oxytocin in APP/PS1 mice and human brain organoid models

AimsTo investigate the therapeutic effects and mechanisms of Semaglutide in Alzheimer's disease (AD), and identify its potential targets. MethodsWe systematically evaluated the effect of Semaglutide on Alzheimer's disease (AD), using both mice and human organoid models. ResultsBehavioral analyses on APP/PS1 mice demonstrated that Semaglutide improved the cognitive capabilities, particularly in the learning and memory domains. Biochemical investigations further highlighted its role in reducing amyloid plaque deposition and down-regulating the expression of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) expression in the mouse brain tissues. Meanwhile, oxytocin (OXT) was up-regulated after Semaglutide treatment. Subsequent studies using human AD-brain organoids (BOs) models revealed that, upon Semaglutide treatment, these AD-BO models also exhibited reduced levels of amyloid-beta (Aβ), phosphorylated Tau (p-Tau) and GFAP expression as well as increased OXT level. ConclusionsSemaglutide can ameliorate Alzheimer's disease in pre-clinical models, suggesting the promising therapeutic potential in AD patients.

Effects of Environmental Noise Stress on Mouse Metabolism

Environmental noise is associated with various health outcomes. However, the mechanisms through which these outcomes influence behavior and metabolism remain unclear. This study investigated how environmental noise affects the liver, adipose tissue, and brain metabolic functions, leading to behavioral and body weight changes. Mice were divided into a noise group exposed to construction noise and an unexposed (control) group. Behavior and body weight changes were monitored over 50 days. Early changes in response to noise exposure were assessed by measuring plasma cortisol and glial fibrillary acidic protein expression in brain tissues on days 1, 15, and 30. Chronic responses, including changes in lipoprotein and fat metabolism and neurotransmitters, were investigated by analyzing serum lipoprotein levels and body fat mass and evaluating liver, fat, and brain tissue after 50 days. The noise group showed higher locomotor activity and reduced anxiety in the open-field and Y-maze tests. Noise exposure caused an initial weight loss; however, chronic noise increased fat mass and induced adipocyte hypertrophy. Our findings underscore the role of environmental noise-induced stress in augmenting locomotor activity and reducing anxiety in mice through neurotransmitter modulation while increasing the risk of obesity by decreasing HDL cholesterol levels and promoting adipocyte hypertrophy.

Folic acid ameliorates high glucose–induced neurotoxicity in human forebrain organoids: Insights from proteomics

AbstractPregestational diabetes (PGDM) has been associated with an elevated risk of congenital abnormalities, particularly those affecting the nervous system. The efficacy of folic acid (FA) supplementation in reducing the incidence of neurodevelopmental damage caused by PGDM has been well documented. However, the exact mechanism is unclear. Here, a human forebrain organoid model, which replicates the three‐dimensional structure of the early fetal neural tissue, was employed to study the neuroprotective effects of FA in PGDM. In this study, the forebrain organoids were cultured at high glucose (HG) concentrations from Days 20 to 40 with or without FA. Immunostaining revealed that the supplementation of FA significantly decreased HG‐induced neuron apoptosis. The proteomics examination suggested HG caused an increase in glial fibrillary acidic protein expression, a marker of astrocytes, leading to the upregulation of metallothionein expression and perturbation of mineral absorption, whereas FA reversed this effect. Proteomics analysis further showed that FA reduced HG‐induced cell migration. Moreover, Western blot analysis verified that FA mitigated HG‐induced apoptosis and cell migration via AMPK/FOXO pathway. Overall, current findings indicate that FA, as a functional food ingredient, has a protective effect on HG‐induced abnormal fetal neurodevelopment.

Impact of Epstein-Barr Virus Nuclear Antigen 1 on Neuroinflammation in PARK2 Knockout Mice.

This study aimed to explore the intricate relationship between mitochondrial dysfunction, infection, and neuroinflammation, focusing specifically on the impact of pathogenic epitopes of the Epstein-Barr Virus (EBV) nuclear antigen 1 (EBNA1) in a mouse model of mitochondrial dysfunctions. The investigation included female middle-aged PARK2-/- and C57BL/6J wild-type mice immunized with EBNA1386-405 or with active experimental autoimmune encephalomyelitis (EAE) induction by the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. The PARK2-/- mice developed more severe EAE than the wild-type mice. Following immunization with EBNA1386-405, only PARK2-/- exhibited symptoms resembling EAE. During the acute phase, PARK2-/- mice immunized with either MOG35-55 or EBNA1386-405 exhibited a similar infiltration of the T cells and macrophages in the spinal cord and decreased glial fibrillary acidic protein (GFAP) expression in the brain. However, the EBNA1386-405 -immunized PARK2-/- mice showed significantly increased frequencies of CD8a+ T cells and CD11c+ B cells, and distinct cytokine profiles in the periphery compared to the wild-type controls. These findings highlight the role of EBV in exacerbating inflammation, particularly in the context of mitochondrial deficiencies.

Evaluation of the Choroid Plexus Epithelium Inflammation TLR4/NF-κB/NKCC1 Signal Pathway Activation in the Development of Hydrocephalus.

Hydrocephalus is characterized by secretion, circulation, and absorption disorder of cerebrospinal fluid (CSF) with high morbidity and complication rate. The relationship between inflammation and abnormal secretion of CSF by choroid plexus epithelium (CPE) had received more attention. In this study, we aim to detect the role of Toll-like receptor 4/nuclear factor-kappa B/Na+/K+/2Cl-cotransporter 1(TLR4/NF-κB/NKCC1) signal pathway in the development of hydrocephalus. Hydrocephalus was induced in adult rats (8 weeks) by intracisternal kaolin injection, then pyrrolidinedithiocarbamate (PDTC) and bumetanide were administrated to the rats mode. Then the rat model was evaluated, and ventricular volume was calculated at different time points. Then CPE, cortex, preventricular tissue, and CSF were obtained. Protein expressions of TLR-4, NKCC/serine-threonine STE20/SPS1-related, proline-alanine-rich kinase (SPAK), pNKCC1, pSPAK, GFAP, AQP1, and AQP4 were measured by RT-PCR, western blot, and immunofluorescence (IF) stains in CPE, respectively. Our data showed that inflammation factors tumor necrosis factor-(TNF-α), interleukin 18(IL-18), and glial fibrillary acidic protein (GFAP) concentrations were significantly higher in the model group than in controls. The TLR4/NF-κB/NKCC1 signal pathway were actived by NF-κB-p65, NKCC1, pNKCC1- pSPAK complex, and Aquaporin1 (AQP1) high expression. PDTC and bumetanide use can help regular TLR4/NF-κB/NKCC1 expression and reduced AQP1 expression by down-regulate NF-B-p65 and inhibiting NKCC1, respectively. As a result, the treatment groups alleviated CPE abnormal secretion and ventricle enlargement. These results confirmed that the inflammatory reaction contributes TLR4/NF-κB/NKCC1 mediated CPE abnormal secretion and consequent hydrocephalus. Regulation of TLR4/NF-κB/NKCC1 and AQP1 can prevent this process. Our study provides a strong rationale for further exploring alleviating CPE abnormal secretion as a therapeutic perspective of hydrocephalus.

Regulatory role of electroacupuncture on satellite glial cell activity in the colon and dorsal root ganglion of rats with irritable bowel syndrome.

To investigate the role of satellite glial cells in irritable bowel syndrome (IBS) and the effect of electroacupuncture (EA) at the Tianshu (ST25) and Shangjuxu (ST37) combination. A model for visceral hypersensitivity in IBS was induced through colorectal distension (CRD) stimulation. Clean-grade male Sprague-Dawley (SD) rats were randomly divided into four groups: a normal group (NG), a model group (MG), an electroacupuncture group (EA), and a glial cell inhibitor group (FCA). Bilateral EA (2/100 Hz, 1 mA, 30 min) was administered at the Tianshu (ST25) and Shangjuxu (ST37) in week 6. Abdominal withdrawal reflex (AWR) scores were used to assess the behavioral response associated with visceral hyperalgesia, while hematoxylin-eosin staining was employed to evaluate pathological changes in the colon. The protein and mRNA levels of glial fibrillary acidic protein (GFAP) in the colon and colon-related dorsal root ganglion (DRG) were analyzed using immun-ofluorescence, immun-ohistochemistry, Western blotting, real-time polymerase chain reaction. The impact of EA on electrophysiological properties of colon-related DRG neurons was observed through whole-cell patch clamp analysis. EA significantly reduced the visceral pain behavior scores in rats with IBS in response to graded (20, 40, 60, 80 mm Hg) CRD stimulation. Additionally, EA downregulated the protein and mRNA expression levels of GFAP in the colon and colon-related DRG of rats with IBS. EA also regulated the resting membrane potential, rheobase and action potential of colon-related DRG neurons in rats with IBS. EA can regulate the excitatory properties of colon-related DRG neurons by downregulating the protein and mRNA expression of GFAP in the colon and colon-related DRG, indicating a potential neurobiological mechanism by which EA relieves visceral hypersensitivity in rats with IBS.

A Systematic Review of Delta-9-Tetrahydrocannabinol (∆9-THC) in Astrocytic Markers.

Astrocytic reactivity in substance use disorders (SUDs) has been extensively studied, yet the molecular effect of delta-9-tetrahydrocannabinol (∆9-THC, the main psychoactive compound in cannabis) on glial cells, especially astrocytes, remains poorly understood. Exploring ∆9-THC's impact on astrocytic markers can provide insight into its effects on brain functions such as homeostasis, synaptic transmission, and response to neuronal injury. This systematic review synthesizes findings from studies investigating ∆9-THC's impact on astrocytic markers. A systematic review was conducted using EMBASE, Medline, and PsychoInfo via the OvidSP platform. Studies reporting astrocytic markers following ∆9-THC exposure in animals and humans were included. Data were extracted from twelve eligible full-text articles, and the risk of bias was assessed using the Systematic Review Center for Laboratory Animal Experimentation. This research identified several astrocytic markers, including glial fibrillary acidic protein (GFAP), nestin, and glutamate-aspartate transporter (GLAST). Both GFAP and nestin expressions increased in adulthood following adolescence and adult ∆9-THC exposure. An increase in GLAST expression was also noted during early development after ∆9-THC exposure. This review indicates varying levels of astrocytic reactivity to ∆9-THC across different developmental stages, including adolescence and adulthood. ∆9-THC appears to impact maturation, particularly during early developmental stages, and exhibits sex-dependent effects.

Co-exposure to different bacterial species’ lipopolysaccharides with the NASH diet exacerbates NASH and liver fibrosis progression in mice

Background and aimWith the obesity epidemic, nonalcoholic fatty liver disease (NAFLD) has become a public health concern, but its progression mechanism remains unclear. Experimental models mimicking human NAFLD/steatohepatitis (NASH) are crucial. This study simulates gut microbiota imbalance effects on NASH and liver fibrosis. MethodsWe used different bacterial sources of lipopolysaccharide (LPS), including Escherichia coli (GEC) and Salmonella abortus equi (GSE), combined with a Gubra Amylin NASH (GAN) diet to induce NASH and liver fibrosis. ResultsThe GSE group showed significantly higher serum alanine aminotransferase, hydroxyproline, CD68-positive cells, α-smooth muscle actin, glial fibrillary acidic protein, and TNF-α, COL1A1, TGF-β, and NLRP3 expressions compared to the the GAN group. The GSE group also had higher Erysipelotrichaceae, Akkermansiaceae, and Bacteroidaceae family numbers. ConclusionsThe GAN diet with LPS treatment successfully induced NASH and fibrosis making this model useful for preclinical NASH drug testing.

Temperature control during pars plana vitrectomy.

To evaluate the impact of temperature-controlled pars plana vitrectomy (PPV) on structural and functional outcomes in a rabbit eye model in vivo. Ten healthy New Zealand White rabbits underwent temperature-controlled PPV in the right eye (group A), using a device specifically designed to heat the infusion fluid/air and integrated into the vitrectomy machine, and conventional PPV in the left eye (group B). Both eyes received ophthalmic examination and electroretinography (ERG) before and 1week postoperatively. After 1-week ERG, rabbits were enucleated and then sacrificed. Histological and immunohistochemical examinations were performed on enucleated eyes and expression of glial fibrillary acidic protein (GFAP) and vimentin investigated. Postoperatively, only group B showed significantly decreased amplitude and increased latency of a-wave at 3cd·s/m2 (p = 0.001 and 0.005, respectively). Significant increase of b-wave latency at 0.01cd·s/m2 was detected in both groups (p = 0.019 and 0.023, respectively). Postoperatively, amplitude of oscillatory potentials (OPs) increased significantly in group A (p = 0.023) and decreased in group B. In both groups, OPs latency significantly increased at 1-week test (P < 0.05). A greater number of eyes without structural retinal alterations was detected in group A compared to group B (6 vs 5, respectively). GFAP expression was higher in group B than group A, even if the difference was not statistically significant. Temperature-controlled PPV resulted in more favorable functional and structural outcomes in rabbit eyes compared with conventional PPV, supporting the potential beneficial role of the intraoperative management of intraocular temperature in vitreoretinal surgery.

Early life seizures and olfactory communication in rats.

Early life seizures (ELS) are commonly associated with autism spectrum disorder (ASD); however, the exact role of ELS in the pathology is unknown. Prior studies have demonstrated social deficits, a core feature of ASD, following ELS; consequently, alterations in sensory modalities may contribute to the overall social deficits. Considering the speculated contribution of sensory deficit to social communication, we examined the developmental consequences of early postnatal kainic acid (KA)-induced seizures on olfactory preference and neural markers in the olfactory bulb in both male and female Sprague Dawley rats. KA-induced seizures or saline was administered. Rats were then exposed to a series of biologically relevant scents including male scent, female scent, nest scent, and phenylethylamine during the juvenile period and again during adulthood. Alterations in sensory modalities were expected to be expressed via abnormal preference for certain scents and/or production of abnormal ultrasonic vocalizations in response to scents. The olfactory bulbs were also assessed for the biologically relevant markers glial fibrillary acidic protein (GFAP) and calcium/calmodulin-dependent protein kinase II (CAMKII). Our findings resulted in no significant differences in olfactory preference following ELS for juveniles or adults compared to controls. Similarly, there were no differences in GFAP expression or the ratio of phosphorylated CAMKII to CAMKII in either olfactory bulb. Interestingly, despite a lack of treatment differences, different scents were shown to elicit different responses in juvenile rats, yet these differences subsided in adulthood. Overall, the results of this study suggest that olfaction does not contribute to socialization deficit following ELS within the KA model.

Chinese Herbs for Inducing Rat Bone Marrow Mesenchymal Stem Cells Differentiated into Neuron-Like Cells

The purpose of this study was to observe the influence of two Chinese herbs of ligustrazine and Xuefuzhuyu injection on neuron-like cells differentiation from rat bone marrow mesenchymal stem cells (BMSCs) respectively. Most primarily cultured BMSCs adhered to the wall at 3 days after cultured, which proliferated faster after passaged, and the 5th passage of cells were mostly purified into BMSCs. In the present study, the 5th passage of BMSCs were (97.51±1.22) % CD44 positive, but negative for CD45, which were identified by immunocytochemical technique. Serum-free low-sugar Dulbecco’s modified Eagle’s medium (L-DMEM) contains 1.25 g/L ligustrazine and 3.0 g/L Xuefuzhuyu injection were used to induce the 5th passage of BMSCs respectively in vitro. Neuron-like cells with prominence and bifurcation could be detected after induction under an inverted phase contrast microscope. The immunocytochemical method showed that nestin and neuron-specific enolase (NSE) were positive in neuron-like cells, but without glial fibrillary acidic protein (GFAP) expression. Both ligustrazine and Xuefuzhuyu injection have the potential for inducing neuron-like cells differentiation from rat bone marrow mesenchymal stem cells respectively. Compared with Xuefuzhuyu injection-induced cells, neuron-like cells induced with ligustrazine might be better in the level of morphological changes, as well as nestin and NSE expression.