Product Name	AGEs
Chinese Name	晚期糖基化终末产物抗体
Alias	advanced glycosylation end products; AGE.
literatures	Specific References  (17)     |     SL1158R has been referenced in 17 publications. [IF=14.593] Wanyi Zhou. et al. Glucose and MMP-9 dual-responsive hydrogel with temperature sensitive self-adaptive shape and controlled drug release accelerates diabetic wound healing. Bioact Mater. 2022 Jan;:  IF ;  Rat.   PubMed:10.1016/j.bioactmat.2022.01.004 [IF=7.169] Zou Ting-feng. et al. Fisetin treatment alleviates kidney injury in mice with diabetes-exacerbated atherosclerosis through inhibiting CD36/fibrosis pathway. ACTA PHARMACOL SIN. 2023 May;:1-10  IF,WB ;  Mouse.   PubMed:37225845 [IF=7.129] Juanjuan Duan. et al. Benzo[a]pyrene and a high-fat diet induce aortic injury and promote low-density lipoprotein accumulation in the endothelium. ECOTOX ENVIRON SAFE. 2023 Jul;259:115011  IHC ;  Mouse.   PubMed:37196526 [IF=6.78] Zhuozhou Hu. et al. Acyclovir alleviates insulin resistance via activating PKM1 in diabetic mice. LIFE SCI. 2022 Sep;304:120725  WB ;  Mouse.   PubMed:35751919 [IF=6.312] Hee-Weon Lee. et al. Glyoxal-Lysine Dimer, an Advanced Glycation End Product, Induces Oxidative Damage and Inflammatory Response by Interacting with RAGE. Antioxidants-Basel. 2021 Sep;10(9):1486  WB ;  Mouse.   PubMed:10.3390/antiox10091486 [IF=6.208] Haiyan Zhou. et al. Glycation of Tie-2 Inhibits Angiopoietin-1 Signaling Activation and Angiopoietin-1-Induced Angiogenesis. INT J MOL SCI. 2022 Jan;23(13):7137  IHC ;  Human.   PubMed:35806141 [IF=6.147] Dedert Cass. et al. Progranulin Preserves Autophagy Flux and Mitochondrial Function in Rat Cortical Neurons Under High Glucose Stress. FRONT CELL NEUROSCI. 2022 Jul;0:354  WB ;  Rat.   PubMed:35880011 [IF=5.27] Huang, Kaipeng, et al. "Sirt1 resists AGEs-induced expressions of FN and TGF-β1 by activating the Nrf2/ARE pathway in GMCs." Free Radical Biology and Medicine (2013).  WB ;  Rat.   PubMed:23891678 [IF=5.151] Kim DY et al. Eucalyptol Inhibits Advanced Glycation End Products‐Induced Disruption of Podocyte Slit Junctions by Suppressing Rage‐Erk‐C‐Myc Signaling Pathway.Mol Nutr Food Res. 2018 Oct;62(19):e1800302.  WB&IHC-P ;  Mouse.   PubMed:29987888 [IF=4.082] Eun-Jung Leeet al. Coumarin Ameliorates Impaired Bone Turnover by Inhibiting the Formation of Advanced Glycation End Products in Diabetic Osteoblasts and Osteoclasts. Biomolecules . 2020 Jul 15;10(7):1052.  WB ;  mouse.   PubMed:32679814 [IF=3.75] Andressa S. Sousa. et al. Evaluation of coronary function in female rats with severe type 1 diabetes: Effects of combined treatment with insulin and pyridoxamine. MICROVASC RES. 2022 Dec;:104474  WB ;  Rat.   PubMed:36592817 [IF=3.571] Oh H et al. Asaronic Acid Attenuates Macrophage Activation toward M1 Phenotype through Inhibition of NF-κB Pathway and JAK-STAT Signaling in Glucose-Loaded Murine Macrophages. J Agric Food Chem. 2019 Aug 26.  WB ;  Mouse.   PubMed:31422663 [IF=3.352] Wei-Yu Yeh. et al. Functional chicken-liver hydrolysates ameliorate insulin resistance and cognitive decline in streptozotocin-induced diabetic mice. Poultry Sci. 2022 Mar;:101887  WB ;  Mouse.   PubMed:10.1016/j.psj.2022.101887 [IF=3.21] Tanaka M et al. Effects of combined treatment with blood flow restriction and low intensity electrical stimulation on diabetes mellitus-associated muscle atrophy in rats.J Diabetes. (2018) Sep 18  WB ;  Calf.   PubMed:30225988 [IF=2.66] Ye, Ruidong, et al. "Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats." Neurochemistry international 58.3 (2011): 391-398.  WB ;  Rat.   PubMed:21185898 [IF=1.39] Ryuma Haraguchi et al. New Insights into the Pathogenesis of Diabetic Nephropathy: Proximal Renal Tubules Are Primary Target of Oxidative Stress in Diabetic Kidney. Acta Histochem Cytochem . 2020 Apr 28;53(2):21-31.  IHC ;  mouse.   PubMed:32410750 [IF=1.11] Lu, Lin, et al. "Effects of atorvastatin on progression of diabetic nephropathy and local RAGE and soluble RAGE expressions in rats." Journal of Zhejiang University SCIENCE B 12.8 (2011): 652-659.  WB ;  Rat.   PubMed:21796806
Research Area	Cell biology  immunology  Diabetes
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	Human, Mouse, Rat,
Applications	WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1ug/Test IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Cellular localization	Secretory protein
Form	Liquid
Concentration	1mg/ml
immunogen	AGEs
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	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. SWISS: P02769 Gene ID: AGEs 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Diabetes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The nucleus因子-κB（NF—κB）的活化，同时这一作用还诱导了cell factor、生长因子及黏附分子表达的增加。 在Diabetes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Diabetes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Diabetes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Extracellular matrix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cell factor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Diabetes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。
Product Picture	Sample: Lane 1: Kidney (Mouse) Tissue Lysate at 40 ug Lane 2: Lung (Mouse) Tissue Lysate at 40 ug Lane 3: Large intestine (Mouse) Tissue Lysate at 40 ug Lane 4: Testis (Rat) Tissue Lysate at 40 ug Lane 5: Lung (Rat) Tissue Lysate at 40 ug Lane 6: Large intestine (Rat) Tissue Lysate at 40 ug Lane 7: U87MG (Human) Cell Lysate at 30 ug Primary: Anti-AGEs (SL1158R) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution Observed band size: 62 kD Tissue/cell: Rat kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded; Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining Tissue/cell: rat kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded; Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-AGEs Polyclonal Antibody, Unconjugated(SL1158R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining Blank control: MCF7. Primary Antibody (green line): Rabbit Anti-AGEs antibody (SL1158R) Dilution: 1μg /10^6 cells; Isotype Control Antibody (orange line): Rabbit IgG . Secondary Antibody : Goat anti-rabbit IgG-AF647 Dilution: 1μg /test. Protocol The cells were incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.

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