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AGEs

AGEs的相关文献在1998年到2022年内共计228篇,主要集中在内科学、中国医学、基础医学 等领域,其中期刊论文144篇、专利文献84篇;相关期刊108种,包括健康大视野、中药药理与临床、中医药信息等; AGEs的相关文献由741位作者贡献,包括吴茜、周梦舟、徐宁等。

AGEs—发文量

期刊论文>

论文:144 占比:63.16%

专利文献>

论文:84 占比:36.84%

总计:228篇

AGEs—发文趋势图

AGEs

-研究学者

  • 吴茜
  • 周梦舟
  • 徐宁
  • 柳志杰
  • 冯年捷
  • 胡勇
  • 汪超
  • 唐诗淼
  • 刘易斯·S·格鲁伯
  • 许惠琴
  • 期刊论文
  • 专利文献

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    • 谈江莹; 陈紫婷; 秦佳斌; 王伊琳; 吴茜
    • 摘要: 本文分析添加莲原花青素(lotus seedpod procyanidins,LSPC)对华夫饼晚期糖化终末产物(advanced glycation end products,AGEs)的抑制及感官品质的影响。以面粉、鸡蛋等为原料,添加不同浓度LSPC(0、0.5、1、2、4 mg/g)并制备华夫饼(170°C,20 min),通过测量华夫饼中AGEs含量、羧甲基赖氨酸含量(N^(ε)-(Carboxymethyl)lysine,CML)、抗氧化性等指标检测LSPC对华夫饼中AGEs的抑制作用;通过色度,质构,气质,电子鼻等方法检测LSPC对华夫饼感官品质的影响。结果表明,华夫饼中AGEs含量和CML含量随LSPC浓度的增加而显著减少(P<0.05),总酚含量随LSPC浓度的增加而显著增加(P<0.05);华夫饼抗氧化性能随LSPC浓度的增加而显著增加(P<0.05);LSPC的添加也影响了华夫饼的焙烤品质,华夫饼的硬度显著下降(P<0.05),弹性和凝聚性显著性增强(P<0.05);华夫饼的色泽显著加深(P<0.05);风味随莲原花青素的添加显著增加(P<0.05)。本研究表明莲原花青素对华夫饼中AGEs有抑制作用,感官品质上使华夫饼口感更绵软可口,同时本文为深入研究莲原花青素对食品热加工过程中AGEs的抑制作用及感官品质的影响提供理论支撑。
    • Shiming Li; Liang Zhang; Xiaochun Wan; Jianfeng Zhan; Chi-Tang Ho
    • 摘要: Myriad evidence attests to the health-promoting benefits of tea drinking.While there are multiple factors of tea influencing the effective biological properties,tea polyphenols are the most significant and valuable components.The chemical characterization and physical characteristics of tea polyphenols have been comprehensively studied over the previous years.Still the emergence of new chemistry in tea,particularly the property of scavenging reactive carbonyl species(RCS)and the newly discovered flavoalkaloid compounds,has drawn increasing attention.In this review,we summarize recent findings of a new class of compounds in tea-flavonoid alkaloids(flavoalkaloids),which exist in fresh tea leaves and can be generated during the process of post-harvesting,and also postulate the formation mechanism of flavoalkaloids between catechins and theanine-derived Strecker aldehyde.Additionally,we detail the up-to-date research results of tea polyphenols regarding their ability to trap RCS and their in vivo aminated metabolites to suppress advanced glycation ends products(AGEs).We further raise questions to be addressed in the near future,including the synthetic pathways for the generation of flavoalkaloids and AGEs in fresh tea leaves before processing and the concentrations of tea polyphenols that affect their RCS scavenging capability due to their pro-oxidant nature.More intensive research is warranted to elucidate the mechanisms of action underlying the biological activity of flavoalkaloids and the pharmacological application of tea polyphenols in scavenging RCS and impeding detrimental AGEs.
    • 张燕
    • 摘要: 以晚期糖基化终末产物(AGEs)与抗糖饮食、糖尿病的联系为情境,以血糖的平衡及其调节为主要考查内容命制综合性试题,分析试题对稳态与平衡观、实验设计能力、批判性思维等核心素养的考查.
    • 刘艳秋; 侯改霞; 习雪峰; 王勇
    • 摘要: 目的:观察和探讨游泳运动在干预2型糖尿病大鼠海马形态结构和认知功能中的作用及可能机制.方法:雄性SD大鼠分为正常组(C)、糖尿病组(D)、糖尿病运动组(DS).DS组大鼠进行无负重游泳运动,每周运动5d,休息2d,干预共12周.HE染色观察大鼠海马CA1区锥体细胞的形态结构,新物体识别实验评价大鼠学习记忆,免疫组织化学检测海马CA1区AGEs含量,Western blot检测大鼠海马RAGE、NOX2的蛋白表达,RT-PCR检测海马NF-κB mRNA表达,比色法检测大鼠海马MDA、GSSG/GSH.结果:与正常组(C组)相比,2型糖尿病大鼠(D组)海马CA1区的锥体细胞排列紊乱,细胞肿胀,胶质细胞增生,细胞间隙增宽等;海马CA1区AGEs集聚增多(P<0.01),海马RAGE和NOX2蛋白表达增多(P<0.01),海马MDA、GSSG/GSH显著升高(P﹤0.01),NF-κB mRNA表达显著升高(P<0.01),糖尿病大鼠认知指数(RI)显著降低(P<0.01).与糖尿病组(D组)相比,游泳运动降低了2型糖尿病大鼠海马CA1区AGEs的集聚(P﹤0.05),海马RAGE和NOX2蛋白表达下降(P﹤0.05),海马MDA、GSSG/GSH显著下降(P﹤0.05或P<0.01),NF-κB mRNA表达下降(P﹤0.05),糖尿病大鼠海马CA1区的锥体细胞的形态结构趋于正常,糖尿病大鼠认知指数(RI)得到提高(P﹤0.05).结论:12周游泳运动在改善糖尿病大鼠认知功能及海马形态结构方面起着一定的作用,其机制可能与运动可以降低2型糖尿病大鼠海马CA1区AGEs的集聚,进而减弱AGEs/RAGE/NOX2/氧化应激/NF-κB信号通路有关.
    • 焦淑玲; 权科佳; 何孝文; 毋卓; 曾宝平; 南禧辰; 杨阳
    • 摘要: 晚期糖基化终末产物(Advanced Glycation End-products,AGEs)是蛋白质、氨基酸等大分子物质在非酶促条件下经美拉德反应形成的化学危害产物。长期食用高热量、高温油炸食物,长期吸烟和长期久坐等都会造成人体AGEs堆积。AGEs在体内堆积会提高骨折风险,引起炎症和糖尿病及其并发症。检测人体AGEs对以上疾病的预防、诊断和治疗具有指导意义。目前用于检测AGEs的方法有酶联免疫法(ELISA法)、光谱法和色谱法等,本文对晚期糖基化终末产物的检测方法进行了综述,为各类检测方法的广泛应用提供借鉴依据。
    • 吴剑; 张柘; 陈沼飞; 刘艳西; 秦星星; 石振
    • 摘要: 目的 观察AGEs调节NF-κB通路对软骨细胞炎症因子IL-1β表达的影响.方法 将软骨细胞传代培养,取对数生长的软骨细胞接种于96孔板,分为对照组、低剂量AGEs(20μg/L)组、高剂量AGEs(40μg/L)组、NF-κB通路抑制剂PDTC(5μg/L)组和AGEs(40μg/L)+PDTC(5μg/L)组,共培养24 h后ELISA检测各组上清液中IL-1β的含量,Real-time PCR检测各组IL-1β和P65基因表达,Western-blot检测IL-1β和P65蛋白表达.结果 对照组软骨细胞上清液中IL-1β的浓度明显高于低剂量AGEs组和高剂量AGEs组,差异有统计学意义(P<0.05);PDTC组和AGEs+PDTC组软骨细胞上清液中IL-1β含量与对照组比较明显下降(P<0.05).对照组软骨细胞中IL-1β和P65 mRNA相对表达量高于低剂量组和高剂量组(P<0.05),低于PDTC组(P<0.05).PDTC组IL-1β和P65 mRNA相对表达量低于AGEs+PDTC组(P<0.05).对照组软骨细胞中IL-1β和P65蛋白相对表达量低于低剂量组和高剂量组(P<0.05),但高于PDTC组(P<0.05).PDTC组软骨细胞中IL-1β和P65蛋白相对表达量较AGEs+PDTC组减少(P<0.05).结论 AGEs上调软骨细胞IL-1β的表达,NF-κB通路可能是参与骨关节炎发生发展的重要通路之一.
    • 焦淑玲; 权科佳; 何孝文; 毋卓; 曾宝平; 南禧辰; 杨阳
    • 摘要: 晚期糖基化终末产物(Advanced Glycation End-products,AGEs)是蛋白质、氨基酸等大分子物质在非酶促条件下经美拉德反应形成的化学危害产物.长期食用高热量、高温油炸食物,长期吸烟和长期久坐等都会造成人体AGEs堆积.AGEs在体内堆积会提高骨折风险,引起炎症和糖尿病及其并发症.检测人体AGEs对以上疾病的预防、诊断和治疗具有指导意义.目前用于检测AGEs的方法有酶联免疫法(ELISA法)、光谱法和色谱法等,本文对晚期糖基化终末产物的检测方法进行了综述,为各类检测方法的广泛应用提供借鉴依据.
    • Kaitlyn Broz; Remy E.Walk; Simon Y.Tang
    • 摘要: Type 2 diabetes mellitus(T2D)is an increasingly prevalent disease with numerous comorbidities including many in the spine.T2D is strongly linked with vertebral fractures,intervertebral disc(IVD)degeneration,and severe chronic spinal pain.Yet the causative mechanism for these musculoskeletal impairments remains unclear.The chronic hyperglycemic state in T2D promotes the formation of advanced glycation end-products(AGEs)in tissues,and the accumulation of AGEs may play a role in musculoskeletal complications by modifying the extracellular matrix,impairing cellular homeostasis,and perpetuating an inflammatory cascade via its receptor(RAGE).The AGE and RAGE associated alterations in extracellular matrix composition and morphological features of the vertebral bodies and IVDs are likely contributors to the incidence and severity of spinal pathologies in T2D.This review will broadly examine the effects of AGEs on tissues in the spine in the context of T2D,with an emphasis on the changes in the vertebrae and the IVD.Along with the clinical and epidemiological findings,we will provide an overview of preclinical rodent models of T2D that exhibit deficits in the IVD and vertebral bone.Elucidating the role of AGEs and RAGE will be crucial for understanding the disease mechanisms and translation therapies of musculoskeletal pathologies in T2D.
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