Biochemistry and Biotechnology Laboratory, CSIR-Central Leather Research Institute, Adyar, Chennai, 600 020, India.
University of Madras, Chepauk, Chennai, 600 005, India.
Appl Biochem Biotechnol. 2022 Jan;194(1):339-353. doi: 10.1007/s12010-021-03762-y. Epub 2021 Dec 2.
Advanced glycation end products (AGEs) formed through non-enzymatic glycosylation between a protein and sugar molecule are highly harmful to the human body. In hyperglycemic patients, AGE formation is more due to high glucose circulating in the blood, causing inter and intra molecular cross-linking of collagen leading to reduction of collagen elasticity. This cross-linked collagen develops resistance to matrix metalloproteinases leading to impaired collagen turnover. The aim of this work is to determine the anti-glycation effects of polydatin and p-coumaric acid in preventing collagen cross-linking by incubating rat tail tendons (RTTs) as collagen source in high glucose concentration (50 mM) for a week. The RTTs were then characterized for tensile strength, cross-linking efficiency, circular dichroism spectrometry, collagen, glucose, and aldehyde contents. Electrophoresis was carried out to evaluate the level of cross-linking in collagen and the results confirmed the ability of the drugs in preventing complex intermolecular cross-link formation induced by non-enzymatic glycosylation. CD data showed alteration in the secondary structure of collagen where AGE formation had occurred. More collagen was extracted by pepsin from RTTs treated with glucose alone (6.88 mg/10 mg tendon) when compared with drug-treated groups (4.25, 2.56 mg/10 mg tendon for polydatin and p-coumaric acid, respectively). Tensile strength (20.66% and 18.95%), cross-linking percentage (32.5% and 29.84%), and glucose content (2.3 and 1.8 mg/100 mg) of drug-treated groups were similar to the positive control (19.07%, 30.13%, and 2.61 mg/100 mg) thus proving the anti-glycation potential of the drugs. Hence, both polydatin and p-coumaric acid could play a pivotal role in preventing AGE formation.
糖基化终产物（AGEs）是蛋白质和糖分子之间非酶糖化反应形成的，对人体有很大危害。在高血糖患者中，AGE 的形成更多是由于血液中葡萄糖含量高，导致胶原分子内和分子间交联，从而降低胶原的弹性。这种交联的胶原对基质金属蛋白酶产生抗性，导致胶原更新受损。本工作旨在通过在高葡萄糖浓度（50mM）下孵育大鼠尾腱（RTT）作为胶原源一周，确定白藜芦醇和对香豆酸对防止胶原交联的抗糖化作用。然后对 RTT 进行拉伸强度、交联效率、圆二色性光谱、胶原、葡萄糖和醛含量的特征分析。电泳用于评估胶原中的交联水平，结果证实了药物在防止非酶糖化诱导的复杂分子间交联形成方面的能力。CD 数据显示胶原二级结构发生变化，AGE 形成。与药物处理组（白藜芦醇和对香豆酸分别为 4.25、2.56mg/10mg 肌腱）相比，单独用葡萄糖处理的 RTT 中提取的胶原量更多（6.88mg/10mg 肌腱）。拉伸强度（20.66%和 18.95%）、交联百分比（32.5%和 29.84%）和葡萄糖含量（2.3 和 1.8mg/100mg）与阳性对照（19.07%、30.13%和 2.61mg/100mg）相似，这证明了药物的抗糖化潜力。因此，白藜芦醇和对香豆酸都可以在防止 AGE 形成方面发挥关键作用。
