ANALYTICA CHIMICA ACTA
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2026
·
IF 6.1
Mengyue Wang,Jinyang Wu,Chengcheng Wang,Dongyu Liu,Ying Wang,Peng Zhao
Ischemic stroke (IS) demands ultra-early diagnosis to improve outcomes, yet conventional imaging modalities often fail to capture the critical window for intervention due to inherent temporal delays. Here, we report a surface-enhanced Raman scattering (SERS)-based plasmonic nanosensor that leverages gold hexagonal nanoparticles (GHNPs) as high-efficiency plasmonic amplifiers to enable simultaneous quantification of two key IS biomarkers-S100β and brain natriuretic peptide (BNP)-directly in whole blood. By engineering a sandwich immunoassay on a silver nanoparticle-modified conductive substrate, the GHNPs generate dense plasmonic “hotspots” that substantially amplify Raman signals, allowing for sensitive and stable detection without sample pretreatment. The sensor was validated in a rat middle cerebral artery occlusion (MCAO) model, capturing dynamic biomarker elevations within hours post-ischemia, and in clinical blood samples from IS patients, where biomarker levels were significantly elevated compared to healthy controls. The platform achieved detection limits as low as 7.18 fg/mL for S100β and 8.98 fg/mL for BNP, markedly outperforming conventional ELISA. By enabling rapid, multiplexed, and highly accurate quantification of these two complementary biomarkers, our SERS platform directly addresses the diagnostic gap between biochemical onset and clinical imaging, offering a powerful tool for ultra-early IS diagnosis and clinical stratification with strong potential for translational application.
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高影响因子
ACS Applied Nano Materials
·
2024
·
IF 5.3
Feng Gao,Yanjiao Wang,Minyue Wang,Chengcheng Wang,Tianwei Wang,Jingguo Wu,Qingbin Ni,Baoliang Sun,Jingyi Sun,Ying Wang
Traumatic brain injury (TBI), serving as a global health problem, is the primary cause of death and disability. However, the lack of a simple, accurate, and rapid method to diagnose and distinguish the injury severity of TBI in the acute phase and further improve the prognosis has been plaguing clinicians. To solve this problem, a highly sensitive surface-enhanced Raman spectroscopy (SERS) sensor, which was based on gold nanorod (AuNR) arrays, has been designed for the quantitative determination of TBI biomarkers. To create this effective SERS sensor, the AuNRs were fabricated via optimizing the particle morphology and, by evaporative self-assembly, optimizing AuNRs were assembled on microsilicon wafers to form AuNR array platforms with an enhancement factor of 1.24 × 106 and a limit of detection reaching 10–2 fg·mL–1. The ideal SERS sensors were further proven to have excellent sensitivity and reliability after being employed to analyze the various levels of S100β and IL-10 both in animal model blood samples and human blood samples. All results revealed that our biosensors can be a promising strategy for point-of-care clinical diagnosis and TBI severity distinction.
研究领域:
生物医学工程
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纳米技术
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分析化学
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临床诊断
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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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PubMed
高影响因子
CNS Neuroscience & Therapeutics
·
2023
·Vol. 29
·期 4
·1000-1011
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IF 5.5
Di Zhang,Bei Jing,Zhen-ni Chen,Xin Li,Hui-mei Shi,Ya-chun Zheng,Shi-quan Chang,Li Gao,Guo-ping Zhao
Introduction Sciatica causes intense pain. No satisfactory therapeutic drugs exist to treat sciatica. This study aimed to probe the potential mechanism of ferulic acid in sciatica treatment. Methods Thirty-two SD rats were randomly divided into 4 groups: sham operation, chronic constriction injury (CCI), mecobalamin, and ferulic acid. We conducted RNA sequencing, behavioral tests, ELISA, PCR, western blotting, and immunofluorescence analysis. TAK-242 and JSH23 were administered to RSC96 and GMI-R1 cells to explore whether ferulic acid can inhibit apoptosis and alleviate inflammation. Results RNA sequencing showed that TLR4/NF-κB pathway is involved in the mechanism of sciatica. CCI induced cold and mechanical hyperalgesia; destroyed the sciatic nerve structure; increased IL-1β, IL-6, TNF-α, IL-8, and TGF-β protein levels and IL-1β, IL-6, TNF-α, TGF-β, TLR4, and IBA-1 mRNA levels; and decreased IL-10 and INF-γ protein levels and IL-4 mRNA levels. Immunohistochemistry showed that IBA-1, CD32, IL-1β, iNOS, nNOS, COX2, and TLR4 expression was increased while S100β and Arg-1 decreased. CCI increased TLR4, IBA-1, IL-1β, iNOS, Myd88, p-NF-κB, and p-p38MAPK protein levels. Treatment with mecobalamin and ferulic acid reversed these trends. Lipopolysaccharide (LPS) induced RSC96 cell apoptosis by reducing Bcl-2 and Bcl-xl protein and mRNA levels and increasing Bax and Bad mRNA and IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK protein levels, while ferulic acid inhibited cell apoptosis by decreasing IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK levels and increasing Bcl-2 and Bcl-xl levels. In GMI-R1 cells, Ferulic acid attenuated LPS-induced M1 polarization by decreasing the M1 polarization markers IL-1β, IL-6, iNOS, and CD32 and increasing the M2 polarization markers CD206, IL-4, IL-10 and Arg-1. After LPS treatment, IL-1β, iNOS, TLR4, Myd88, p-p38MAPK, and p-NF-κB levels were obviously increased, and Arg-1 expression was reduced, while ferulic acid reversed these changes. Conclusion Ferulic acid can promote injured sciatic nerve repair by reducing neuronal cell apoptosis and inflammatory infiltration though the TLR4/NF-κB pathway.
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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细胞生物学
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炎症研究
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DOI
PubMed
高影响因子
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