JOURNAL OF THE ELECTROCHEMICAL SOCIETY
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2025
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IF 3.3
Yirong Ma,Min Gong,Xinran Wei,Fan Yang,Yunzhe Li,Guanjun Nan,Zhimin Luo,Aiguo Zeng
A two-step electropolymerization strategy was constructed to establish an electrochemical sensor method for sensitive and selective detection of betamethasone. First, a poly-(2-aminoterephthalic acid) (P(ATA)) layer, which can significantly enhance electronic conductivity, was synthesized on the surface of the bare electrode using electropolymerization. Subsequently, taurine (Tau), which is rich in sulphonate groups, was electropolymerized and introduced into the P(ATA) layer to obtain P(Tau)/P(ATA)/GCE. Then, the electropolymerization parameters and test conditions were optimized, including the concentration of polymerization solution, the scanning rate, the polymerization cycles, buffer pH and accumulation time. Characterization of the obtained electrodes done using scanning electron microscopy and several electrochemical characterization methods proved the successful preparation of the P(Tau)/P(ATA)/GCE. Electrochemical tests of betamethasone at different concentrations (0.2-25μg·mL-1) under optimal measurement conditions exhibited excellent linearity, good sensitivity. Compared with commonly employed HPLC method, the proposed sensor method was much fast, simple, environmentally friendly, and cost-effective. Compared with other sensor methods, P(Tau)/P(ATA)/GCE sensor exhibited good sensitivity and excellent stability. Moreover, the P(Tau)/P(ATA)/GCE sensor was successfully applied to quantitatively detect betamethasone in cosmetics, which provides a new method for the monitoring of illegal addition of glucocorticoids in cosmetics.
研究领域:
分析化学
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材料科学
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环境科学
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产品关联
DOI
高影响因子
JOURNAL OF ALZHEIMERS DISEASE
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2015
·Vol. 49
·期 3
·829-844
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IF 4.151
Shan Ye,Wang Dan-Dan,Xu Yu-Xia,Wang Chu,Cao Lan,Liu Yun-Sheng,Zhu Cui-Qing
Stress is an important risk factor of Alzheimer’s disease (AD). It has been evidenced that stress could induce tau phosphorylation and increase tau insolubility in brain; however, little is known about the interactional effect of stress with aging on tauopathy. Therefore, we explored the effects of aging on stress-induced tauopathy and the potential mechanism in mouse model of chronic restraint stress (CRS). Here we found that in general, the level of phosphorylated tau (P-tau) was higher in brain of middle-aged mice than that in adult mice under physiological conditions. CRS-induced tau phosphorylation and its insolubility were more prominent in middle-aged mice. The increase of AT8-labeled insoluble P-tau was dramatic in middle-aged mice, which was highly ubiquitinated but did not form PHF structures. The levels of chaperones were relatively lower in middle-aged mice brain; CRS further reduced the expression, especially for HDJ2/HSP40. CRS also suppressed the expression of Pin1, the peptidylprolyl cis/trans isomerase, in middle-aged mice but not in adult mice. Downregulation of HSP40 or Pin1 caused an increase of transfected extraneous tau in 293 cells. Rosmarinic acid (RA) could effectively suppress the elevation of P-tau and insoluble P-tau formation induced by CRS, and reversed the abnormal changes of chaperones and Pin1 particularly in middle-aged mice. Taken together, our findings provided evidence that aging could be a promoting factor in stress-induced tauopathy, which was relevant with malregulation of chaperones and Pin1, and RA might be a promising beneficial agent for stress-induced tauopathy.
研究领域:
神经科学
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药理学
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老年学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Cell and Bioscience
·
2024
·Vol. 14
·期 1
·1-18
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IF 6.1
Maimaiti Yasenjiang,Su Ting,Zhang Zhanying,Ma Lingling,Zhang Yuan,Xu Hong
This study investigates NADPH oxidase 4 (NOX4) involvement in iron-mediated astrocyte cell death in Alzheimer’s Disease (AD) using single-cell sequencing data and transcriptomes. We analyzed AD single-cell RNA sequencing data, identified astrocyte marker genes, and explored biological processes in astrocytes. We integrated AD-related chip data with ferroptosis-related genes, highlighting NOX4. We validated NOX4’s role in ferroptosis and AD in vitro and in vivo. Astrocyte marker genes were enriched in AD, emphasizing their role. NOX4 emerged as a crucial player in astrocytic ferroptosis in AD. Silencing NOX4 mitigated ferroptosis, improved cognition, reduced Aβ and p-Tau levels, and alleviated mitochondrial abnormalities. NOX4 promotes astrocytic ferroptosis, underscoring its significance in AD progression.
研究领域:
神经科学
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分子生物学
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基因组学
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神经退行性疾病
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产品关联
DOI
PubMed
高影响因子
Food & Function
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2024
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IF 5.1
Like Lin,Cong Li,Yujiao Zhang,Li Zhang,Lu Gao,Lihua Jin,Yu Shu,Yehua Shen
Akt acts as a central protein influencing multiple pathologies in neurodegenerative diseases including AD and PD, and Akt activators are promising management strategies. The current study characterized the effects of an Akt-activating peptide (Glu-Pro-Glu-Val-Leu-Pro, EPEVLR) obtained from walnut protein degradation on D-gal-induced memory impairment in mice. The EPEVLR was obtained by hydrolysis of walnut proteins, identification of peptide sequences, and screening for molecular docking sequentially. The MWM test in mice indicated that the oral administration of EPEVLR (80, 200 and 400 mg/kg·d) significantly (p < 0.05) reversed D-gal-induced memory impairment. WB tests of the mice hippocampus confirmed that EPEVLR could activate Akt by promoting its phosphorylation. In addition, further characterizations (including TEM, ELISA, and immunohistochemistry) related to Akt phosphorylation observed lower Aβ and p-Tau levels, as well as more autophagosomes than in the model group. Moreover, the EPEVLR treatment significantly increased Lactobacillus and reduced Helicobacter abundance of the gut microbiome, and caused up-regulation of SCFAs and down-regulation of LPS of serum metabolite. Therefore, EPEVLR ingestion reversed cognitive impairment symptoms possibly related to the activation of Akt and regulation of the intestinal flora pathway. Consumption of the EPEVLR diet is beneficial for cognitive dysfunction.
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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胃肠病学
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产品关联
DOI
PubMed
高影响因子
PSYCHOPHARMACOLOGY
·
2024
·
IF 3.5
Liu Xin,Jin Yongzeng,Cheng Xinyi,Song Qinghua,Wang Yanan,He Ling,Chen Tong
Rationale The plasma ceramide levels in Alzheimer’s disease (AD) patients are found abnormally elevated, which is related to cognitive decline. Objectives This research was aimed to investigate the mechanisms of aberrant elevated ceramides in the pathogenesis of AD. Results The ICR mice intracerebroventricularly injected with Aβ 1-42 and APP/PS1 transgenic mice were employed as AD mice. The cognitive deficiency, impaired episodic and spatial memory were observed without altered spontaneous ability. The serum levels of p-tau and ceramide were evidently elevated. The modified expressions and activities of glycogen synthase kinase-3β (GSK-3β) and protein phosphatase 2A (PP2A) influenced the serum content of p-tau. The levels of ceramide synthesis-related genes including sptlc1, sptlc2, cers2, and cers6 in the liver of AD mice were increased, while the ceramide degradation-related gene asah2 did not significantly change. The regulations of these genes were conducted by activated nuclear factor kappa-B (NF-κB) signaling. NF-κB, promoted by free fatty acid (FFA), also increased the hepatic concentrations of proinflammatory cytokines. The FFA amount was modulated by fatty acid synthesis-related genes acc1 and srebp-1c. Besides, the decreased levels of pre-proopiomelanocortin (pomc) mRNA and increased agouti-related protein (agrp) mRNA were found in the hypothalamus without significant alteration of melanocortin receptor 4 (MC4R) mRNA. The bioinformatic analyses proved the results using GEO datasets and AlzData. Conclusions Ceramide was positively related to the increased p-tau and impaired cognitive function. The increased generation of ceramide and endoplasmic reticulum stress in the hypothalamus was positively related to fatty acid synthesis and NF-κB signaling via brain–liver axis.
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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病理学
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DOI
PubMed
高影响因子
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