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抗氧化蛋白聚糖对α-葡萄糖苷酶活性和非酶糖基化的抑制作用。

Inhibition on α-Glucosidase Activity and Non-Enzymatic Glycation by an Anti-Oxidative Proteoglycan from .

机构信息

State Key Laboratory of Molecular Engineering of Polymers, Department of Macromolecular Science, Fudan University, Shanghai 200433, China.

Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China.

出版信息

Molecules. 2022 Feb 22;27(5):1457. doi: 10.3390/molecules27051457.

DOI:10.3390/molecules27051457
PMID:35268560
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8912016/
Abstract

The prevention of postprandial hyperglycemia and diabetic complications is crucial for diabetes management. Inhibition of α-glucosidase to slow carbohydrate metabolism is a strategy to alleviate postprandial hyperglycemia. In addition, suppression of non-enzymatic glycation can diminish the advanced glycation end products and reduce the oxidative stress and inflammation, thereby preventing the diabetic complications. In this study, an anti-oxidative proteoglycan (named ) extracted from was investigated in vitro for its inhibitory effect on α-glucosidase and non-enzymatic glycation using molecular kinetics, intrinsic fluorescence assay, and bovine serum albumin glycation models. The molecular kinetics and fluorescence assay revealed that decreases α-glucosidase activity by forming a -α-glucosidase complex. To evaluate the anti-glycation effect, fructose-glycated and methylglyoxal-glycated BSA models were analyzed by spectroscopic and SDS-PAGE methods. Results showed that inhibited the glycation at every stage and suppressed glycoxidation, possibly due to its anti-oxidative capacity and -BSA complex formation. Furthermore, we demonstrated in vivo that could alleviate postprandial hyperglycemia in mice as well as AGE accumulation and vascular injury in diabetic rats. Overall, possesses anti-postprandial hyperglycemia and anti-glycation functions and would be potentially used in clinic for diabetes and related complication management.

摘要

预防餐后高血糖和糖尿病并发症对于糖尿病管理至关重要。抑制α-葡萄糖苷酶以减缓碳水化合物代谢是缓解餐后高血糖的一种策略。此外,抑制非酶糖化可以减少晚期糖基化终产物,减轻氧化应激和炎症,从而预防糖尿病并发症。在这项研究中,我们研究了从 中提取的一种抗氧化糖胺聚糖(命名为 ),以评估其对 α-葡萄糖苷酶和非酶糖化的抑制作用,采用分子动力学、内源荧光测定法和牛血清白蛋白糖化模型。分子动力学和荧光测定法表明 通过形成 -α-葡萄糖苷酶复合物来降低α-葡萄糖苷酶的活性。为了评估抗糖化作用,我们通过光谱和 SDS-PAGE 方法分析了果糖糖化和甲基乙二醛糖化 BSA 模型。结果表明, 在各个阶段都抑制了糖化作用,并抑制了糖基化氧化,这可能归因于其抗氧化能力和 -BSA 复合物的形成。此外,我们在体内证明 可以减轻 小鼠的餐后高血糖以及糖尿病大鼠的 AGE 积累和血管损伤。总的来说, 具有抗餐后高血糖和抗糖化功能,有望在临床上用于糖尿病及其相关并发症的管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/4bdcdd78dcdf/molecules-27-01457-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/9c7c8b0352ee/molecules-27-01457-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/60527c46f0d0/molecules-27-01457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/db9bbb32a59d/molecules-27-01457-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/ae1f74ef73ed/molecules-27-01457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/239e2cb9334a/molecules-27-01457-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/26427c6c3056/molecules-27-01457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/393241271fbf/molecules-27-01457-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/36a3547a6156/molecules-27-01457-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/981d10997fdb/molecules-27-01457-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/4bdcdd78dcdf/molecules-27-01457-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/9c7c8b0352ee/molecules-27-01457-g001a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/60527c46f0d0/molecules-27-01457-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/db9bbb32a59d/molecules-27-01457-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/ae1f74ef73ed/molecules-27-01457-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/239e2cb9334a/molecules-27-01457-g005a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/26427c6c3056/molecules-27-01457-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/393241271fbf/molecules-27-01457-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/36a3547a6156/molecules-27-01457-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/981d10997fdb/molecules-27-01457-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e888/8912016/4bdcdd78dcdf/molecules-27-01457-g010.jpg

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