ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2023
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IF 6.8
Juanjuan Duan,Hong Li,Yu Wang,Yongchao Ji,Chao Chen,Chengqiang Feng,Wensheng Zhang
Benzo[a]pyrene (BaP) is a ubiquitous environmental pollutant which mainly exposed though diet. High-fat diet (HFD) can induce atherosclerosis, as can BaP. Unhealthy dietary habits lead to high intake of both BaP and lipids. However, the combined effect of BaP and HFD on atherosclerosis and lipid accumulation in the arterial wall, the initial stage of atherosclerosis, is unclear. In this study, C57BL/6 J mice were subchronically exposed to BaP and a HFD, and the mechanism of lipid accumulation was investigated in EA.hy926 and HEK293 cells. Results showed that BaP and HFD increased blood lipids and damaged aortic wall synergistically. Meanwhile, LDL enhanced the toxicity of BaP, and BaP promoted the production of reactive oxygen species and malonaldehyde in EA.hy926 cells, which aggravated LDL-induced cell injury. Moreover, BaP and HFD/LDL induced LDL accumulation in the aortic wall of C57BL/6 J mice/EA.hy926, and the mechanism was by activating AHR/ARNT heterodimer to combine with the scavenger receptor BⅠ (SR-BⅠ) and activin receptor-like kinase 1 (ALK1) promoter regions to transcriptional upregulate its expression, which enhanced the uptake of LDL, and promoting the production of AGEs to inhibit reverse cholesterol transport by SR-BI. BaP and lipid synergistically promoted aortic and endothelial damage, and the health risk of their combined intake should be paid attention to.
研究领域:
毒理学
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心血管疾病
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环境健康
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
LWT-FOOD SCIENCE AND TECHNOLOGY
·
2022
·
IF 6.056
Xin Xu,Tian Xue,Qingqing Jiang,Daming Fan,Mingfu Wang,Yueliang Zhao
The inhibitory effects of four hydrocolloids, including alginic acid, pectin, carboxymethylcellulose sodium salt, and chitosan on the formation of two typical toxic advanced glycation end products N Ɛ -(carboxymethyl) lysine (CML) and N Ɛ -(carboxyethyl) lysine (CEL) were investigated in chemical models and fish patties. All the four hydrocolloids were found to significantly inhibit CML and CEL formation in chemical models, and among them, pectin and alginic acid were the most effective inhibitors. In roast fish patties, the addition of pectin and alginic acid at 0.9% reduced the content of CML by 43.6% and 44.9%, and CEL by 32.4% and 32.6%, respectively. Moreover, alginic acid plus a polyphenol epigallocatechin gallate (EGCG) showed stronger inhibitory effect against CML and CEL formation than alginic acid alone. Further study showed that alginic acid and pectin decreased the formation of glyoxal (GO) and methylglyoxal (MGO), two key intermediates of CML and CEL, in the chemical models and fish patties. In addition, compared with EGCG, the addition of alginic acid in fish patties showed less impact on color, odor, and sensory properties. These findings suggest that alginic acid is a potent inhibitor against the formation of AGEs with less impact on food quality.
研究领域:
食品科学
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化学
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营养学
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产品关联
DOI
高影响因子
Advanced Fiber Materials
·
2025
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IF 21.3
Li Chao,Li Wentao,Deng Ronghui,Huang Lingan,Song Yifan,Wei Xianjie,Xu Bingbing,Cui Guoqing,Chen Zehao,Yu Jiakuo
Excessive interface friction and advanced glycation end products (AGEs) disrupt collagen ordered deposition, promoting scar formation in tendinopathies. Inspired by tendon sheath anatomy, we developed a bionic bilayer nano-membrane via electrospinning and photocrosslinking to initiate the directional and orderly regeneration process of tendon tissue. The lubricating layer (PP), containing phosphatidylserine (PS), reduces frictional stress, while the regenerative layer (GM/GV), composed of gelatin methacrylate (GM) and vanillin-modified gelatin (GV), scavenges ROS and mitigates AGEs-induced collagen disorder deposition. This parallel bilayer structure guides tendon cell alignment and promotes ordered collagen deposition. Additionally, vanillin suppresses the AGEs/TGF-β/Smad pathway, reducing scar formation and tissue adhesion. In vitro/in vivo tests showed a fivefold decrease in coefficient of friction (COF) and a tenfold increase in Achilles tendon function index (AFI) compared to the PCL and normal groups, respectively. The PP@GM/GV membrane, regulated by mechano-biochemical coupling factors, offers a promising strategy for tendinopathy repair, and holds significant potential for clinical translation in guiding functional tendon regeneration and improving patient outcomes. Graphical
研究领域:
生物医学工程
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组织工程
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再生医学
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生物材料
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骨科
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产品关联
DOI
高影响因子
GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
·
2022
·Vol. 261
·期 3
·735-748
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IF 3.535
Li Zhen,Han Yu,Ji Yan,Sun Kexin,Chen Yanyi,Hu Ke
Purpose Oxidative stress and inflammation had been proved to play important role in the progression of diabetic keratopathy (DK). The excessive accumulation of AGEs and their bond to AGE receptor (RAGE) in corneas that cause the formation of oxygen radicals and the release of inflammatory cytokines, induce cell apoptosis. Our current study was aimed to evaluate the effect of ALA on AGEs accumulation as well as to study the molecular mechanism of ALA against AGE-RAGE axis mediated oxidative stress, apoptosis, and inflammation in HG-induced HCECs, so as to provide cytological basis for the treatment of DK. Methods HCECs were cultured in a variety concentration of glucose medium (5.5, 10, 25, 30, 40, and 50 mM) for 48 h. The cell proliferation was evaluated by CCK-8 assay. Apoptosis was investigated with the Annexin V- fluorescein isothiocyanate (V-FITC)/PI kit, while, the apoptotic cells were determined by flow cytometer and TUNEL cells apoptosis Kit. According to the results of cell proliferation and cell apoptosis, 25 mM glucose medium was used in the following HG experiment. The effect of ALA on HG-induced HCECs was evaluated. The HCECs were treated with 5.5 mM glucose (normal glucose group, NG group), 5.5 mM glucose + 22.5 mM mannitol (osmotic pressure control group, OP group), 25 mM glucose (high glucose group, HG group) and 25 mM glucose + ALA (HG + ALA group) for 24 and 48 h. The accumulation of intracellular AGEs was detected by ELISA kit. The RAGE, catalase (CAT), superoxide dismutase 2 (SOD2), cleaved cysteine-aspartic acid protease-3 (Cleaved caspase-3), Toll-like receptors 4 (TLR4), Nod-like receptor protein 3 (NLRP3) inflammasome, interleukin 1 beta (IL-1 ß), and interleukin 18 (IL-18) were quantified by RT-PCR, Western blotting, and Immunofluorescence, respectively. Reactive oxygen species (ROS) production was evaluated by fluorescence microscope and fluorescence microplate reader. Results When the glucose medium was higher than 25 mM, cell proliferation was significantly inhibited and apoptosis ratio was increased ( P < 0.001). In HG environment, ALA treatment alleviated the inhibition of HCECs in a dose-dependent manner, 25 μM ALA was the minimum effective dose. ALA could significantly reduce the intracellular accumulation of AGEs ( P < 0.001), activate protein and genes expression of CAT and SOD2 ( P < 0.001), and therefore inhibited ROS-induced oxidative stress and cells apoptosis. Besides, ALA could effectively down-regulate the protein and gene level of RAGE, TLR4, NLRP3, IL-1B, IL-18 ( P < 0.05), and therefore alleviated AGEs-RAGE-TLR4-NLRP3 pathway–induced inflammation in HG-induced HCECs. Conclusion Our study indicated that ALA could be a desired treatment for DK due to its potential capacity of reducing accumulation of advanced glycation end products (AGEs) and down-regulating AGE-RAGE axis–mediated oxidative stress, cell apoptosis, and inflammation in high glucose (HG)–induced human corneal epithelial cells (HCECs), which may provide cytological basis for therapeutic targets that are ultimately of clinical benefit.
研究领域:
眼科学
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细胞生物学
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分子生物学
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糖尿病
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产品关联
DOI
PubMed
高影响因子
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