RSC Advances
·
2019
·Vol. 9
·期 70
·40887-40894
·
IF 3.049
Xue Yang,Ke Ma,Libo Yang,Yujuan Chen,Yingmin Qu,Ying Wang,Xinyue Wang,Fan Yang,Qi Sun,Zhengxun Song,Zuobin Wang
This paper employs a spin-coated method to construct conductive polypyrrole (PPy) substrates which present superior properties for controlling the morphological structures and functions of bEnd.3 cells. The PPy substrates with a homogeneous particle size, uniform distribution and proper roughness show enhanced hydrophilic characteristics and improve cell adhesion to the substrates. The changes in the mechanical properties of cells and the responses to the designed substrates and magnetic field are also explored. Due to the synergistic effect between the magnetic field and the conductive PPy substrate, the cells cultured in such an environment exhibit applanate shapes with more branches and enhanced cell viability. In addition, the cells preferentially extend along the magnetic field direction. The mechanical characteristics of cells change significantly under varying magnetic intensity stimulations (5–16 mT). The satisfying effect on cells' morphology and outgrowth is acquired at the magnetic intensities of 9–10 mT and duration of 20 min, compared with other stimulated groups, while retaining cell viability. Moreover, the cells express higher adhesion up to 5.2 nN. The results suggest that the application of the PPy substrates and magnetic field is a promising candidate for the protection of neurovascular units and treatment of neurological diseases.
研究领域:
生物医学工程
·
神经科学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
·
2025
·Vol. 39
·期 9
·e70453
·
IF 2.8
Dongfang Hu,Zihui Shen,Xueke Hou,Zhishuai Wan,Xiaoyu Guo,Lingli Chen,Zhihong Yin,Hongmei Ning,Yaming Ge
Florfenicol (FLO), a widely used antibiotic, can cause early embryonic death and impaired angiogenesis. However, the mechanism by which FLO inhibits angiogenesis and its role in FLO-induced embryonic toxicity are not yet fully understood. This study aimed to investigate the effect of FLO on the proliferation and migration of mouse bEnd.3 endothelial cells (bECs) and the underlying mechanism, given the crucial role of endothelial cells in angiogenesis. The results showed that FLO treatment at 7.5–15 μg/mL significantly inhibited proliferation and migration in a time-dependent manner, with stronger effects observed after 48 h compared to 24 h. RNA sequencing analysis identified 1351 genes differentially expressed in response to FLO. Functional analysis indicated that FLO disrupted ATP metabolism, angiogenesis, vasculature development, and actin filament organization. The F-actin cytoskeleton remodeling was morphologically confirmed, and activation of the ROCK/Cofilin signaling pathway was detected. Subsequent experiments demonstrated that pharmacological inhibition of the pathway normalized cytoskeletal rearrangement and promoted angiogenesis, as evidenced by enhanced wound closure and increased cell viability. Our results demonstrated that ROCK-mediated F-actin remodeling plays a crucial role in the FLO-induced inhibition of proliferation and migration in bECs. These findings may explain why FLO inhibited angiogenesis. However, further investigations are necessary to validate our findings in in vivo experiments.
研究领域:
药理学
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细胞生物学
·
分子生物学
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毒理学
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发育生物学
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DOI
PubMed
高影响因子
JOURNAL OF ASIAN NATURAL PRODUCTS RESEARCH
·
2020
·
IF 1.345
Min-Ye Huang,Gu-Ran Yu
This study aimed to evaluate the effect Cycloastragenol (CAG), a triterpenoid saponin isolated from the Radix astragali, on Aβ-induced BBB damage. An immortalized endothelial cell line (bEnd.3) was employed to mimic a BBB. The Western blot, TUNEL staining, Flow cytometric analysis and Enzyme-linked immunosorbent assay were performed. The present results showed that CAG (10, 50, 75 μM) can alleviate oligomer Aβ1–42 induced bEnd.3 cell apoptosis and increase tight junction scaffold proteins expression. The result also indicated that CAG increased soluble Aβ efflux across BBB via upregulation of the P-gp and downregulation of RAGE expression.
研究领域:
神经科学
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药理学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2022
·
IF 5.318
Jiaqi Lu,Jinxia Chen,Chunyan Yang,Chen Xia,Junling Deng,Zuoya Xiang,Jian Chen,Yong Wu
Epigallocatechin-3-gallate (EGCG) is a polyphenol naturally sourced in green tea with extensive bioactivities, including antioxidant, anti-carcinogenic, anti-microbial, anti-obesity, and neuroprotection. However, EGCG is unstable in neutral or alkaline conditions and has poor lipid solubility , leading to inadequate systemic absorption, reduced pharmacokinetics , limited biodistribution , and first-pass metabolism. The aim of this study is to solve these problems, thus two novel EGCG-glucose conjugates , Glu-EGCG and 2Glu-EGCG possessing one and two glucose, respectively, were designed, synthesized, and characterized. The EGCG-glucose conjugates’ chemical stability, cytotoxicity and alleviation H 2 O 2 -induced antioxidative damage to neuronal cell and antioxidative neuroprotection activities were examined. Compared with their precursor EGCG, Glu-EGCG and 2Glu-EGCG are more stable, less toxic to PC12 and bEnd.3 cell, stronger ability to attenuate H 2 O 2 -induced injury to PC12 cells resulting higher cell viability and lower reactive oxygen species (ROS) in the cell. Animal study results further proved that Glu-EGCG and 2Glu-EGCG possess higher antioxidative activities than EGCG, through decreasing the ischemia area, inhibiting morphological changes and neuronal loss in brain tissues, and modulating the oxidative factor and antioxidant factor. In conclusion, 2Glu-EGCG shows stronger antioxidant activities than Glu-EGCG does. Both EGCG-glucose conjugates are promising brain target antioxidative neuroprotection agents.
研究领域:
药理学
·
神经科学
·
生物化学
·
分子生物学
✓ 已验证
DOI
高影响因子
Human Cell
·
2024
·
IF 3.4
Cao Yue,Xing Ruixian,Li Qiushi,Bai Yang,Liu Xuewen,Tian Buxian,Li Xin
Reperfusion after cerebral ischemia leads to secondary damage to the nervous system, called cerebral ischemia/reperfusion injury (CIRI). The blood–brain barrier (BBB) consists of endothelial cells and tight junction (TJ) proteins, and its disruption aggravates CIRI. Two GSE datasets identified Tissue Factor Pathway Inhibitor 2 (TFPI2) as a differentially upregulated gene (Log2FC > 1, p < 0.01) in the cerebral cortex of ischemic rats, and TFPI2 affects angiogenesis of endothelial cells. Moreover, genes (c-Jun, c-Fos, FosL1) encoding subunits of Activator Protein-1 (AP-1), a transcription factor involved in IRI, were highly expressed in ischemic samples. Thus, the effects of the AP-1/TFPI2 axis on CIRI were explored. We determined increased TFPI2 expression in the cerebral cortex of rats receiving middle cerebral artery occlusion (MCAO) for 90 min and reperfusion (R) for 48 h. Then AAV2-shTFPI2 particles (5 × 10 10 vg) were injected into the right lateral ventricle of rats 3 weeks before MCAO/R. TFPI2 knockdown decreased infarct size and neuronal injury in ischemic rats. It improved BBB integrity, demonstrated by reduced FITC-dextran leakage in brain tissues of MCAO/R-operated rats. Furthermore, it increased the expression of TJ proteins (Occludin, Claudin-5, TJP-1) in the cerebral cortex of rats with CIRI. Consistently, we found that TFPI2 knockdown mitigated cell damage in mouse endothelial bEND.3 cells with oxygen and glucose deprivation (ODG) for 6 h and reoxygenation (R) for 18 h (OGD/R) treatment. High co-expression of c-Jun and c-Fos significantly elevated TFPI2 promoter activity. c-Jun knockdown inhibited TFPI2 expression in OGD/R-treated bEND.3 cell. Collectively, our findings demonstrate that inhibition of the AP-1/TFPI2 axis alleviates CIRI.
研究领域:
神经科学
·
分子生物学
·
细胞生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
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