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首页> 外文期刊>African Journal of Biotechnology >Inhibition of protein glycation and advanced glycation end products by ascorbic acid
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Inhibition of protein glycation and advanced glycation end products by ascorbic acid

机译：抗坏血酸抑制蛋白质糖基化和高级糖基化终产物

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Advanced glycation end products (AGEs) formation is increased in diabetes mellitus, leading to?microvascular and macrovascular complications.?Recently, much attention has been focused on natural and synthetic inhibitors to delay the onset or progression of diabetes and its comorbidities. Ascorbic acid (AA) can react with proteins, including hemoglobin and possibly interfere with protein glycation process.?An?in vitro?glycation model containing plasma from type 2 diabetic and non-diabetic healthy volunteers together with glucose as glycating agent was used to study antiglycation activity of AA. Samples with different concentrations of glucose and AA were incubated for five weeks at 37°C. Nonenzymatic glycation (NEG) was quantitated by thiobarbituric acid calorimetry and AGEs were measured by enzyme linked immuno-sorbent assay (ELISA). The NEG and AGEs levels were reduced by AA. Increasing the AA concentrations greatly diminished protein glycations, indicating dose-dependent effects of AA. Plasma NEG and AGEs were decreased with an average of 20 to 26% (p < 0.05) and 26 to 28% (p < 0.05). A significant correlation was found between the glycation inhibition and the inhibition of AGE formation (p < 0.05). The antiglycation role of AA is evident in the present study and it also indicates the possibility of inexpensive, relatively non-toxic vitamin therapy for the prevention and treatment of diabetic complications. It is plausible that AGEs inhibition by AA may also form the basis for future intervention strategies in both diabetic and non-diabetic individuals.
机译：糖尿病中晚期糖基化终产物（AGEs）的形成增加，从而导致“微血管和大血管并发症”。近来，人们对天然和合成抑制剂的关注集中于延缓糖尿病及其合并症的发作或发展。抗坏血酸（AA）可以与包括血红蛋白在内的蛋白质发生反应，并可能干扰蛋白质的糖基化过程。采用体外葡萄糖化模型，该模型包含2型糖尿病和非糖尿病健康志愿者的血浆以及葡萄糖作为糖化剂AA的抗糖化活性。将具有不同浓度的葡萄糖和AA的样品在37°C下孵育5周。通过硫代巴比妥酸量热法对非酶糖基化（NEG）进行定量，并通过酶联免疫吸附测定（ELISA）测量AGEs。 AA降低了NEG和AGEs水平。增加AA浓度会大大减少蛋白质糖基化，表明AA具有剂量依赖性。血浆NEG和AGEs平均降低20％至26％（p <0.05）和26％至28％（p <0.05）。发现糖基化抑制与AGE形成的抑制之间存在显着相关性（p <0.05）。 AA的抗糖化作用在本研究中很明显，它还表明了预防和治疗糖尿病并发症的廉价，相对无毒的维生素疗法的可能性。可能的是，AA抑制AGEs也可能构成未来对糖尿病和非糖尿病患者进行干预策略的基础。

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