| 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 |
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Specific References (13) | bs-1158P has been referenced in 13 publications.
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| 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(xiàng) | 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(jī)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(xì)胞核因子-Kap B（NF—Kap B）的活化，同時這一作用還誘導(dǎo)了細(xì)胞因子、生長因子及黏附分子表達(dá)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(jī)械強(qiáng)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(jī)體，如引起血管通透性增大、血管基底膜增厚和細(xì)胞外基質(zhì)積聚等。AGEs與其細(xì)胞表面受體（RAGE）結(jié)合，通過趨化和活化單核巨噬細(xì)胞，激活轉(zhuǎn)錄因子NF-KB，促進(jìn)細(xì)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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