Frontiers in Pharmacology
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2025
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IF 4.8
Tianyao Li,Jiaxin Chen,Zhouyuan Xie,Jiansong Fang,Qiqing Wu,Xinyue Cao,Ziying Chen,Yiyun Wang,Qiqi Fan,Qi Wang,Jinman Liu
Introduction Ginseng, known as the “king of herbs,” has long been used in traditional Chinese medicine due to its beneficial properties, including anti-aging, anti-inflammatory, and anti-apoptotic effects. Ginsenosides, the active compounds in ginseng, have shown promise in treating neurodegenerative diseases such as Alzheimer’s disease (AD). This study investigates the therapeutic potential of Ginsenoside Ro and its underlying mechanisms in AD treatment. Methods In this study, male APP/PS1 transgenic mice were divided into five groups and treated with Ginsenoside Ro or ginseng for one month. Cognitive function and anxiety were assessed through behavioral tests, including the open field test (OFT) and Morris water maze (MWM). To evaluate Aβ deposition, neuronal apoptosis, neuroinflammation, and the MAPK pathway, various techniques were employed: Thioflavin-T staining, Nissl staining, immunofluorescence, Western blot, and qRT-PCR analyses. Results Ginsenoside Ro significantly improved cognitive function and reduced anxiety in APP/PS1 mice. It also decreased Aβ deposition and ameliorated neuronal apoptosis in the cerebral cortex. The treatment regulated the expression of pro-apoptotic proteins (Bax and Caspase3) and increased the anti-apoptotic protein Bcl-2. Additionally, Ginsenoside Ro reduced neuroinflammation by decreasing IBA1-positive microglia and GFAP-positive astrocytes and lowering pro-inflammatory cytokines while enhancing anti-inflammatory cytokine IL-10. Furthermore, the phosphorylation levels of p38 and JNK in the MAPK pathway were significantly reduced, suggesting a key mechanism for its therapeutic effects. Discussion These findings provide strong evidence supporting Ginsenoside Ro as a potential therapeutic agent for Alzheimer’s disease. Its effects appear to be mediated through the modulation of the IBA1/GFAP-MAPK pathway, which may offer new insights into AD treatment strategies.
研究领域:
神经科学
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药理学
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中医药
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DOI
PubMed
高影响因子
MICROCHIMICA ACTA
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2024
·Vol. 191
·期 6
·1-15
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IF 5.3
Wang Yupeng,Yu Zhiyong,Ning Zhenqiu,Li Minghui,Li Weiping,Zhong Yizhe,Chen Huiqiang,Zhang Xi,Tang Xialin,Cheng Xiao,Li Laiqing,Aigul Abduldayeva,Zan Jie
Glial fibrillary acidic protein (GFAP) in serum has been shown as a biomarker of traumatic brain injury (TBI) which is a significant global public health concern. Accurate and rapid detection of serum GFAP is critical for TBI diagnosis. In this study, a time-resolved fluorescence immunochromatographic test strip (TRFIS) was proposed for the quantitative detection of serum GFAP. This TRFIS possessed excellent linearity ranging from 0.05 to 2.5 ng/mL for the detection of serum GFAP and displayed good linearity ( Y = 598723 X + 797198, R 2 = 0.99), with the lowest detection limit of 16 pg/mL. This TRFIS allowed for quantitative detection of serum GFAP within 15 min and showed high specificity. The intra-batch coefficient of variation (CV) and the inter-batch CV were both < 4.0%. Additionally, this TRFIS was applied to detect GFAP in the serum samples from healthy donors and patients with cerebral hemorrhage, and the results of TRFIS could efficiently discern the patients with cerebral hemorrhage from the healthy donors. Our developed TRFIS has the characteristics of high sensitivity, high accuracy, and a wide linear range and is suitable for rapid and quantitative determination of serum GFAP on-site. Graphical abstract
研究领域:
生物医学工程
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临床化学
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神经学
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产品关联
DOI
PubMed
高影响因子
INFLAMMOPHARMACOLOGY
·
2024
·
IF 4.6
Weng Jiyu,Wang Ying,Tan Zekai,Yuan Yanghe,Huang Shiyuan,Li Zexi,Li Yiming,Zhang Lanyue,Du Zhiyun
Objectives Chronic neuroinflammation has become one of the important causes of common neurodegeneration disease. Therefore, the target of this study was to explore the protective action of glabridin on lipopolysaccharide (LPS)-induced neuroinflammation in vivo and in vitro and its mechanism. Methods The neuroinflammation model was established by LPS-induced BV2 cells. The cell viability with various concentrations of glabridin was determined by MTT assay, and the content of NO in each group was detected. A neuroinflammatory model was established in male C57BL/6J mice for a water maze test. Subsequently, NF-κB and SOD indices were measured by ELISA, GFAP and IBA-1 indices were measured by immunofluorescence, and Nissl staining was used to explore the Nissl bodies in the hippocampus of mice. Results In vitro experiments, our results expressed that glabridin could markedly increase the cell activity of LPS-induced BV2 cells and reduce the NO expression in cells. It indicated that glabridin had a remarkable impact on the neuroinflammation of LPS-induced BV2 cell protection. In vivo neuroinflammation experiments, mice treated with different doses of glabridin showed significantly improved ability of memory compared with the LPS group in the Morris water maze test. The levels of NF-κB, GFAP, and the number of positive cells in Nissl staining were decreased. High-dose glabridin significantly increased the SOD content in the brain tissue and decreased the IBA-1 levels. Conclusion Glabridin can significantly reduce or even reverse LPS-induced neuroinflammation, which may be related to the fact that glabridin can reduce the NO expression, NF-κB, IBA-1, GFAP, and other inflammatory mediators, upregulate the expression of SOD to relieve oxidative stress of brain and inhibit the activation of gliocyte in brain tissue.
研究领域:
神经科学
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药理学
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免疫学
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细胞生物学
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DOI
PubMed
高影响因子
ARCHIVES OF TOXICOLOGY
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2025
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IF 6.9
Su Ziyang,Kong Rui,Huang Chengqing,Wang Kun,Liu Chenhao,Gu Xiaozhen,Wang Hui-Li
Microplastics exposure can induce brain dysfunction like cognitive impairment, Parkinson's disease, and autism spectrum disorders. In this study, we aimed to investigate the effects of Polystyrene nanoplastics (NPS) on anxiety and depression in mice. First, Polystyrene nanoplastics (NPS) (10 mg/kg) were administered orally daily for two months starting at PND 21. Subsequently, behavioral tests about anxiety and depression were conducted, including the open field test, the elevated plus maze, the forced swimming test, and the tail suspension test. The results showed that NPS induced anxiety and depression-like behaviors in mice. The mPFC played a pivotal role in the etiology of anxiety and depression, in which nanoplastics led to impaired synaptic transmission and reduced neuronal activity in vivo in mPFC. Furthermore, the astrocyte marker GFAP was abnormally increased as observed in mPFC. The abnormal activation of astrocytes results in impaired glutamate recycling through decreasing the expression of the glutamate transporter protein EAAT2 after NPS exposure. In order to ascertain the function of EAAT2, the EAAT2 activator (LDN-212320) was employed to stimulate the expression of EAAT2. Following the activation of EAAT2, synaptic transmission, and anxiety and depressive behavior were rescued in the mice. Polystyrene nanoplastics induce anxiety and depressive-like behavior in mice possibly inhibiting astrocyte EAAT2 expression. Specific activation EAAT2 of astrocytes rescue anxiety and depressive behavior in nanoplastics exposed mice.
研究领域:
神经科学
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环境科学
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心理学
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毒理学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
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2025
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IF 5.9
Pengfei Yan,Junchao Wang,Xiyu Zhao,Liangyu Wang,Jia Xu,Weijia Li,Weihong Min,Dan Wu,Chunlei Liu
QMDDQ is peptide derived from shrimp that ameliorates scopolamine-induced memory impairment. In this study, behavioral experiments in mice showed that QMDDQ could reduce the latency, number of working memory errors of the total distance moved, number of reference memory errors, number of traversals of the original platform, and escape latency in mice. QMDDQ decreased AChE vitality and increased ACh, DA, and 5-HT content. HE staining revealed that the cells in the hippocampal areas exhibited a tight tissue structure, neat arrangement, clear outline, and no cell necrosis in the QMDDQ group. Immunohistochemistry showed that, the expression level of Notch1 protein was reduced, and that of the antibody antigen complex was reduced in the QMDDQ group. Immunofluorescence staining showed a decrease in the number of GFAP and Iba-1 of QMDDQ group. TEM revealed that the mitochondrial cristae are intact and clear of QMDDQ group. QMDDQ decreased expression levels of Notch 1, STAT3, HES1, GFAP, and Iba-1 and activated Notch1 signaling via western-blotting. Pharmacokinetic studies have shown that QMDDQ can be stably absorbed into the bloodstream, with absorption occurring within 12 h and metabolism being completed within 24 h. This study establishes a theoretical basis for active peptides to ameliorate memory impairment and initiates the development of memory-enhancing functional foods.
研究领域:
神经科学
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药理学
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分子生物学
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DOI
高影响因子
DRUG DEVELOPMENT RESEARCH
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2022
·Vol. 83
·期 8
·1758-1765
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IF 5.004
Longxue Cai,Renqing Zeng,Qi Huang,Xianfa Liu,Zuohong Cao,Qicai Guo
Neuropathic pain affects millions of people in the worldwide, but the major therapeutics perform limited effectiveness. Paeonol (PAE) is widely distributed in Paeonis albiflora , and has manifested anti-inflammatory and antioxidative effects in multiple diseases. The present study aims to elucidate the effect of Paeonol (PAE) on neuropathic pain (NP) and the potential targets. Chronic constriction injury model was established to mimic NP in vivo in rats. The expression of GFAP, HDAC2, AHDAC3, Ac-H3K9, Histone-H3, Ac-H4K12, Histone-H4, TNF-α, IL-1β, and IL-6 was assessed by real-time polymerase chain reaction, western blot, and/or enzyme-linked immunosorbent assay kits. Ultimately, results indicated that intervention of PAE significantly blocked neuroinflammation and astrocytic activation via blocking HDAC/miR-15a signaling in CCI rats. These data revealed PAE is a novel therapeutic target for the treatment of neuropathic pain.
研究领域:
药理学
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神经科学
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疼痛管理
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DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
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2023
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IF 3.9
Yan Nan,Wang Zhengdong,Li Zhou,Zheng Yang,Chang Nan,Xu Kangjie,Wang Qian,Duan Xiaoxu
This study aimed to examine the immuntoxic effects of arsenic in the nervous system. Our results showed that arsenic increased corticocerebral and hippocampal weights ( p < 0.05). Morris water maze tests revealed that arsenic significantly increased the time spent in latency to platform on the fourth day in 50 mg/L arsenic exposure and the fifth day in 25 and 50 mg/L arsenic exposure, as well as reduced the path length in target quadrant, time spent in target quadrant, and crossing times of the platform ( p < 0.05). Hematoxylin–eosin staining showed that the vacuolated degeneration and pyknosis was found in the cerebral cortex and hippocampus of arsenic-treated mice. The mRNA levels of corticocerebral and hippocampal brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) were decreased in the 50 mg/L arsenic-treated group ( p < 0.05). In addition, immunofluorescence staining showed that 25 and 50 mg/L arsenic all increased the expression of CD11b and glial fibrillary acidic protein (GFAP) in the cerebral cortex and hippocampus ( p < 0.05). Arsenic markedly raised antigen-presenting molecule MHCII and CD40 mRNA levels in the cerebral cortex and hippocampus and upregulated the cell chemokine receptor 5 (CCR5) and CCR7 mRNA levels in the cerebral cortex at the 50 mg/L arsenic group, and increased the CCR7 mRNA levels in the hippocampus at the 25 and 50 mg/L arsenic groups ( p < 0.05). Arsenic activated the nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome, and enhanced its upstream promoter NF-κB protein level and downstream regulators IL-18 mRNA levels. Collectively, these results provide new evidences for the neuro-immune toxicity of arsenic. Graphical abstract
研究领域:
神经毒理学
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免疫毒理学
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神经科学
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DOI
PubMed
高影响因子
NPG Asia Materials
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2022
·Vol. 14
·期 1
·1-11
·
IF 10.761
Chen Zheng,Wang Lin,Chen Chichi,Sun Jie,Luo Junchao,Cui Wenguo,Zhu Can,Zhou Xiaozhong,Liu Xingzhi,Yang Huilin,Shi Qin
Cell-derived extracellular matrix (ECM) has been applied in spinal cord injury (SCI) regeneration because of its various biological functions. However, insufficient mechanical properties limit its wide application. Herein, we developed GelMA/ECM hydrogel fibrous scaffolds (GelMA/ECM scaffolds) that can recruit and enhance the differentiation of neural stem cells (NSCs) by electrospinning and decellularization techniques. Moreover, the GelMA/ECM scaffolds had good mechanical properties and reinforced cell adhesion and proliferation. Compared to GelMA hydrogel fibrous scaffolds (GelMA scaffolds), GelMA/ECM scaffolds promoted more NSCs toward neurons by markedly enhancing the expression of MAP-2 and Tuj-1 and decreasing GFAP expression. In addition, the GelMA/ECM scaffolds significantly reduced the proportion of M1-phenotype macrophages, which is favorable for SCI repair. In vivo, the GelMA/ECM scaffolds recruited NSCs at the injured site, promoted neuron regeneration, and reduced the formation of glial scars and the inflammatory response, which further led to a significant improvement in the functional recovery of SCI. Therefore, this scaffold shows potential in regenerative medicine, mainly in SCI.
研究领域:
再生医学
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生物医学工程
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神经科学
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组织工程
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产品关联
DOI
高影响因子
Surfaces and Interfaces
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2022
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IF 6.137
Junqi Li,Jingguo Wu,Jixiang Chen,Shan Huang,Jian Liu,Feng Gao,Ying Wang,Baoliang Sun,Dan Yu,Jingyi Sun
Tumor necrosis factor alpha (TNFα) and glial fibrillary acidic protein (GFAP) are candidate biomarkers for early diagnosis and evaluation of spinal cord injury (SCI). In fact, their concentrations in serum, plasma, or cerebrospinal fluid are highly correlated with the SCI severity and neurological prognosis. Therefore, development of a rapid, ultrasensitive, and accurate technique for dual-detection of these important biomarkers is critical for SCI diagnosis, monitoring, and recovery assessment. We synthesized gold nanorods (AuNRs) with stable aspect ratio and fabricated an AuNR array parallelly aligned on a substrate using evaporation-induced self-assembly. The uniform morphology and neat arrangement of the AuNRs produce many hotspots that increase the sensitivity and reproducibility of the array. For dual detection of TNF-α and GFAP, the self-assembled AuNR array substrate was modified with anti-TNFα and anti-GFAP. Then, special Raman probe molecules, specific antibodies, and AuNRs were combined to fabricate surface-enhanced Raman scattering (SERS) tags of [email protected] and [email protected] modified with anti-TNFα and anti-GFAP, respectively. Sandwich immunoassay using standard solutions of TNFα and GFAP provided limits of detection of 0.023 and 0.018 pg/mL, respectively. The detector was evaluated on concentrations of TNFα and GFAP in plasma of SCI rat models. Cross-validation against ELISA (enzyme-linked immunosorbent assay) indicated that the SERS sandwich immunoassay detector based on AuNR array substrate has a high dual-detection accuracy. Overall, the proposed detector provides high sensitivity, reproducibility, stability, and accuracy, and it correctly performs dual detection. The fabricated detector platform seems promising for detection of multiple molecules to achieve early and accurate disease diagnosis in clinical practice.
研究领域:
纳米技术
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生物医学工程
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神经科学
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分析化学
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医学诊断
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产品关联
DOI
高影响因子
MICROCHIMICA ACTA
·
2021
·Vol. 188
·期 12
·1-9
·
IF 5.833
Zhao Peng,Sun Jingyi,Zhao Shijun,Song Yanan,Gao Feng,Wang Hongbin,Ni Qingbin,Wang Ying,Sun Baoliang
A surface-enhanced Raman scattering (SERS)–based immunoassay with gold nanostars (GNSs) is utilized for determination of the subarachnoid hemorrhage (SAH) biomarker glial fibrillary acidic protein (GFAP) at very low concentration levels, which allows for early diagnosis and guides clinical decision-making to treat SAH-induced complications. The Raman reporter 5,5′-dithiobis-2-nitrobenzoic acid (DTNB) modified on GNSs was selected as the SERS tags. The SERS immunoassay was assembled by SERS tag and GFAP probe-immobilized ITO substrate. Therefore, the level of GFAP can be detected by monitoring the characteristic Raman peak intensity of GFAP-conjugated GNSs at 1332 cm −1 with a very low detection limit. Under optimized conditions, the assay can work in the GFAP concentration range from 1 pg⋅mL −1 to 1 μg⋅mL −1 , with a detection limit as low as 0.54 fg⋅mL −1 . The performance of the SERS immunoassay proven by the detection of GFAP is equivalent to that of the conventional enzyme-linked immunosorbent assay (ELISA). Graphical abstract Scheme 1. Schematic illustration of GNSs SERS immunoassay for ultrasensitive dynamic change detection of GFAP. (SAH: Subarachnoid hemorrhage, SCF: Cerebrospinal fluid; GNSs: gold nanostars; SERS: surface-enhanced Raman scattering; GFAP: glial fibrillary acidic protein)
研究领域:
纳米技术
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分析化学
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生物标志物检测
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医学诊断
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产品关联
DOI
PubMed
高影响因子
ARCHIVES OF ORAL BIOLOGY
·
2021
·
IF 2.635
Yujia Cui,Mingru Bai,Daimo Guo,Yueyi Yang,Haoran Chen,Jianxun Sun,Jing Xie,Xuedong Zhou
Objective Insulin-like growth factor 1 (IGF1) is one of the vital factors in regenerative endodontics . Previous studies have focused on the role of IGF1 in the mineralization of dental tissues. However, the role of IGF1 in the neural differentiation of dental stem cells was little discussed. Design IGF1 was overexpressed in human stem cells from the apical papilla (hSCAPs) by lentivirus and knocked down in hSCAPs by small interfering RNA . The neural differentiation level of hSCAPs was investigated histologically by HE staining and Nissl staining after neural induction for 3 days. The expression of proteins was examined by western blot and immunofluorescence. Results IGF1 promoted neural differentiation of hSCAPs, more cell processes and Nissl-positive body stained cells. IGF1 overexpression could both promote glial differentiation in hSCAPs, characterized by the increase of S100β and GFAP proteins, and neuronal differentiation , characterized by the increase of βIII-tubulin and functional GAD67/vGLUT1 proteins. Conversely, IGF1 knockdown suppressed both glial and neuronal differentiation. IGF1 activated AKT to regulate the early neural differentiation of hSCAPs. Conclusions The results indicate IGF1 could promote neural differentiation of hSCAPs by activating AKT signaling and provide a cue for the candidate of induced neural seeding cells in regenerative endodontics.
研究领域:
牙科学
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干细胞生物学
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神经科学
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再生医学
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产品关联
DOI
PubMed
高影响因子
Progress in Orthodontics
·
2024
·Vol. 25
·期 1
·1-13
·
IF 3.5
Chen Wenyuanfeng,Qu Yuan,Liu Yining,Zhang Guorui,Sharhan Hasan M.,Zhang Xinzhu,Zhang Kunwu,Cao Baocheng
Background Orthodontic pain affects the physical and mental health of patients. The spinal trigeminal subnucleus caudalis (SPVC) contributes to the transmission of pain information and serves as a relay station for integrating orofacial damage information. Recently, glial cells have been found to be crucial for both acute and maintenance phases of pain. It has also been demonstrated that rho kinase (ROCK) inhibitors can manage different pain models by inhibiting glial cell activation. Here, we hypothesized that orthodontic pain is related to glial cells in the SPVC, and Fasudil, a representative rho/rock kinase inhibitor, can relieve orthodontic pain by regulating the function of glial cells and the related inflammatory factors. In this study, we constructed a rat model of tooth movement pain and used immunofluorescence staining to evaluate the activation of microglia and astrocytes. Quantitative real-time PCR was used to detect the release of related cytokines and the expression of pain-related genes in the SPVC. Simultaneously, we investigated the effect of Fasudil on the aforementioned indicators. Results In the SPVC, the expression of c-Fos peaked on day 1 along with the expression of OX42 (related to microglial activation), CD16 (a pro-inflammatory factor), and CD206 (an anti-inflammatory factor) on day 3 after tooth movement, followed by a gradual decrease. GFAP-staining showed that the number of activated astrocytes was the highest on day 5 and that cell morphology became complex. After Fasudil treatment, the expression of these proteins showed a downward trend. The mRNA levels of pro-inflammatory factors (IL-1β and TNF-α) peaked on day 3, and the mRNA expression of the anti-inflammatory factor TGF-β was the lowest 3 days after tooth movement. Fasudil inhibited the mRNA expression of pain-related genes encoding CSF-1, t-PA, CTSS, and BDNF. Conclusion This study shows that tooth movement can cause the activation of glial cells in SPVC, and ROCK inhibitor Fasudil can inhibit the activation of glial cells and reduce the expression of the related inflammatory factors. This study presents for the first time the potential application of Fasudil in othodontic pain.
研究领域:
牙科学
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神经科学
·
疼痛管理
·
药理学
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产品关联
DOI
PubMed
高影响因子
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