晚期糖基化终末产物AGEs蛋白/AGEs说明书-分析方法-资讯-生物在线

晚期糖基化终末产物AGEs蛋白/AGEs说明书

作者:上海钰博生物科技有限公司 2023-03-29T00:00 (访问量:213)

 AGEs

晚期糖基化终末产物AGEs蛋白

英文名称 AGEs
中文名称 晚期糖基化终末产物AGEs蛋白
别    名 AGEs  
Specific References  (12)     |     bs-1158P has been referenced in 12 publications.
111 [IF=5.5] Ren X et al. Up-Regulation Thioredoxin Inhibits Advanced Glycation End Products-Induced Neurodegeneration.(2018)Cell Physiol Biochem. 2018;50(5):1673-1686.  CCK-8 assay ;  
111 [IF=2.548] Zhang P et al. AGEs induce epithelial to mesenchymal transformation of human peritoneal mesothelial cells via upregulation of STAT3.Glycoconj J. 2019 Apr;36(2):155-163.  Other ;  
111 [IF=2.965] Meng L et al. Human α defensins promote the expression of the inflammatory cytokine interleukin-8 underhigh-glucose conditions: Novel insights into the poor healing of diabetic foot ulcers. J Biochem Mol Toxicol. 2019 Jun 3:e22351.  Other ;  
111 [IF=4.268] Wang N et al. Timosaponin AIII attenuates inflammatory injury in AGEs-induced osteoblast and alloxan-induced diabetic osteoporosis zebrafish by modulating the RAGE/MAPK signaling pathways. Phytomedicine. 2020 May 24;75:153247.  Other ;  zebrafish.  222
111 [IF=4.044] Jinjuan Lv. et al. Sulforaphane delays diabetes-induced retinal photoreceptor cell degeneration. Cell Tissue Res. 2020 Dec;382(3):477-486  WB ;  Mouse.  222
 
111 [IF=3.269] Xiaohua Sun. et al. Etomidate ameliorated advanced glycation end-products (AGEs)-induced reduction of extracellular matrix genes expression in chondrocytes. Bioengineered. 2021;12(1):4191-4200  WB ;  Human.  222
 
111 [IF=2.629] Zhao Shao-Yang. et al. A Study of the Protective Effect of Bushen Huoxue Prescription on Cerebral Microvascular Endothelia Based on Proteomics and Bioinformatics. Evid-Based Compl Alt. 2022;2022:2545074  Other ;  Other.  222
 
111 [IF=7.658] Wenbo Mao. et al. Phloretin ameliorates diabetes-induced endothelial injury through AMPK-dependent anti-EndMT pathway. PHARMACOL RES. Pharmacol Res. 2022 May;179:106205  Other ;  Other.  222
 
111 [IF=3.009] Tan, Hao. et al. Notch/NICD/RBP-J signaling axis regulates M1 polarization of macrophages mediated by advanced glycation end products. GLYCOCONJUGATE J. 2022 Jun;:1-11  
111 [IF=8.755] Shiyu Lin. et al. Tetrahedral framework nucleic acids-based delivery promotes intracellular transfer of healing peptides and accelerates diabetic would healing. CELL PROLIFERAT. 2022 Jul 09  
 
111 [IF=8.025] Bingfeng Lin. et al. Structural characterization and anti-osteoporosis effect of an arabinomannan from Anemarrhena asphodeloides Bge. INT J BIOL MACROMOL. 2023 Mar;231:123324  Rat.  222
 
111 [IF=6.208] Shengqi Huo. et al. ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury. INT J MOL SCI. 2023 Jan;24(2):1667  Rat.  222
 
 
性    状 Lyophilized or Liquid
物    种 N/A
序    列 Purified native protein
纯    度 >95% as determined by SDS-PAGE
内毒素 Not analyzed
活性 Yes
缓 冲 液 PBS (pH=7.4)
保存条件 Stored at -70℃ or -20℃. Avoid repeated freeze/thaw cycles.
注意事项 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
产品介绍 Advanced Glycation End products (AGEs) are the result of a chain of chemical reactions after an initial glycation reaction. The intermediate products are known, variously, as Amadori, Schiff base and Maillard products, named after the researchers who first described them. (The literature is inconsistent in applying these terms. For example, Maillard reaction products are sometimes considered intermediates and sometimes end products.) Side products generated in intermediate steps may be oxidizing agents (such as hydrogen peroxide), or not (such as beta amyloid proteins).[1] "Glycosylation" is sometimes used for "glycation" in the literature, usually as 'non-enzymatic glycosylation. The AGE modified BSA was produced by reacting BSA with glycolaldehyde under sterile conditions followed by extensive dialysis and purification steps.


AGEs又称非酶糖基化终末产物(AGEs) 是蛋白质、脂质和核酸等大分子的游离氨基与还原性单糖的醛基反应所生成的稳定的共价化合物, 在体内的积累、增多是导致糖尿病等多种疾病及其并发症的关键因素。AGEs的异常增多,可直接或间接地对机体产生致病作用。

晚期糖基化终末产物-AGEs的相关学说
晚期糖基化终末产物(Advanced glycation endproducts,AGEs)是一类经由糖,包括通过Maillard反应形成的代谢中间产物化学修饰的蛋白。AGEs具有高度交联性。 AGE与AGE受体(如RAGE)的相互作用诱导了受体承载细胞核因子-Kap B(NF—Kap B)的活化,同时这一作用还诱导了细胞因子、生长因子及黏附分子表达的增加。
在糖尿病方面,晚期糖基化终末产物(AGEs)可引起体内组织一系列病理生理改变,是导致糖尿病慢性并发症的重要致病因素。在健康人群中AGEs也随年龄增加在组织中持续积累,并参与衰老过程。由于糖尿病和衰老均可导致骨代谢紊乱,甚至出现骨质疏松及脱钙。
AGEs具有广泛的致病作用:AGEs形成后引起蛋白质分子间广泛交联,致使蛋白质结构、机械强度、溶解性和配位结合等性质均发生改变。体内多种蛋白质糖基化可从多个方面影响机体,如引起血管通透性增大、血管基底膜增厚和细胞外基质积聚等。AGEs与其细胞表面受体(RAGE)结合,通过趋化和活化单核巨噬细胞,激活转录因子NF-KB,促进细胞因子和组织因子的释放,灭活一氧化氮和产生氧自由基等途径,参与糖尿病慢性并发症的发生和发展 。由于AGEs的不可逆性,即使高血糖被纠正后,AGEs水平也不能回复到正常,而继续在组织中累积。从组织AGEs自然解释出的反应中间物,如不能经肾脏消除,可再次结合到其他结构上,发生AGEs的“第二次”或“第三次”生成,致病作用加重

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