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AGEs (bs-1158P)  
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產(chǎn)品編號 bs-1158P
英文名稱 AGEs
中文名稱 晚期糖基化終末產(chǎn)物AGEs蛋白
別    名 AGEs  
Specific References  (13)     |     bs-1158P has been referenced in 13 publications.
[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  
[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.  
[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.  
[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.  
[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 ;  
[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.  
[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.  
[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.  
[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  
[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 ;  
[IF=2.885] Yi Xiaowei. et al. NLRP10 promotes AGEs-induced NLRP1 and NLRP3 inflammasome activation via ROS/MAPK/NF-κB signaling in human periodontal ligament cells. ODONTOLOGY. 2023 Apr;:1-12  
[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.  
[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 ;  
理論分子量 kDa
檢測分子量
性    狀 Lyophilized or Liquid
物    種 N/A
序    列 Purified native protein
純    度 >95% as determined by SDS-PAGE
內(nèi)毒素 Not analyzed
活性 Yes
緩 沖 液 PBS (pH=7.4).
保存條件 Stored at -70℃ or -20℃. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
產(chǎn)品介紹 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又稱非酶糖基化終末產(chǎn)物(AGEs) 是蛋白質(zhì)、脂質(zhì)和核酸等大分子的游離氨基與還原性單糖的醛基反應(yīng)所生成的穩(wěn)定的共價化合物, 在體內(nèi)的積累、增多是導(dǎo)致糖尿病等多種疾病及其并發(fā)癥的關(guān)鍵因素。AGEs的異常增多,可直接或間接地對機體產(chǎn)生致病作用。

晚期糖基化終末產(chǎn)物-AGEs的相關(guān)學(xué)說
晚期糖基化終末產(chǎn)物(Advanced glycation endproducts,AGEs)是一類經(jīng)由糖,包括通過Maillard反應(yīng)形成的代謝中間產(chǎn)物化學(xué)修飾的蛋白。AGEs具有高度交聯(lián)性。 AGE與AGE受體(如RAGE)的相互作用誘導(dǎo)了受體承載細胞核因子-Kap B(NF—Kap B)的活化,同時這一作用還誘導(dǎo)了細胞因子、生長因子及黏附分子表達的增加。
在糖尿病方面,晚期糖基化終末產(chǎn)物(AGEs)可引起體內(nèi)組織一系列病理生理改變,是導(dǎo)致糖尿病慢性并發(fā)癥的重要致病因素。在健康人群中AGEs也隨年齡增加在組織中持續(xù)積累,并參與衰老過程。由于糖尿病和衰老均可導(dǎo)致骨代謝紊亂,甚至出現(xiàn)骨質(zhì)疏松及脫鈣。
AGEs具有廣泛的致病作用:AGEs形成后引起蛋白質(zhì)分子間廣泛交聯(lián),致使蛋白質(zhì)結(jié)構(gòu)、機械強度、溶解性和配位結(jié)合等性質(zhì)均發(fā)生改變。體內(nèi)多種蛋白質(zhì)糖基化可從多個方面影響機體,如引起血管通透性增大、血管基底膜增厚和細胞外基質(zhì)積聚等。AGEs與其細胞表面受體(RAGE)結(jié)合,通過趨化和活化單核巨噬細胞,激活轉(zhuǎn)錄因子NF-KB,促進細胞因子和組織因子的釋放,滅活一氧化氮和產(chǎn)生氧自由基等途徑,參與糖尿病慢性并發(fā)癥的發(fā)生和發(fā)展 。由于AGEs的不可逆性,即使高血糖被糾正后,AGEs水平也不能回復(fù)到正常,而繼續(xù)在組織中累積。從組織AGEs自然解釋出的反應(yīng)中間物,如不能經(jīng)腎臟消除,可再次結(jié)合到其他結(jié)構(gòu)上,發(fā)生AGEs的“第二次”或“第三次”生成,致病作用加重。
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