果胶裂解酶修饰的红参提取物具有较强的体内外抗糖基化作用。

Chan-Sik Kim, Kyuhyung Jo, Mi-Kyung Pyo, Jin Sook Kim, Junghyun Kim
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引用次数: 6

摘要

目的:GS-E3D是一种新开发的果胶裂解酶修饰的红参提取物。本研究的目的是评估GS-E3D对晚期糖基化终产物的抑制作用。方法:在体外和链脲霉素诱导的糖尿病大鼠实验中,我们评估了GS-E3D对晚期糖基化终产物(AGEs)的形成及其与胶原交联的抑制作用。结果:体外甲基乙二醛糖基化牛血清白蛋白实验显示,GS-E3D抑制AGE形成的IC50值为19.65±4.35 μg/mL。此外,GS-E3D对AGEs与胶原的交联具有较强的抑制作用(IC50 = 0.42±0.08 mg/mL)。然而,在分解实验中,GS-E3D对与胶原交联的预成型AGEs没有影响。为了确定GS-E3D是否在体内抑制AGE的形成及其与蛋白质的交联,我们采用链脲佐菌素诱导的糖尿病大鼠分别给予GS-E3D(25、50和100 mg/kg/天)治疗6周。给药GS-E3D降低糖尿病大鼠血清AGEs水平及其与蛋白质的交联。结论:该药物对体内外晚期糖基化的抑制作用提示其可能在控制糖尿病诱导的各组织AGE负担方面具有潜在的治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo.

Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo.

Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo.

Pectin lyase-modified red ginseng extract exhibits potent anti-glycation effects in vitro and in vivo.

Purpose: GS-E3D is a newly developed pectin lyase-modified red ginseng extract. The purpose of this study was to evaluate the inhibitory effects of GS-E3D against advanced glycation end products.

Methods: In this study, we evaluated the inhibitory effects of GS-E3D on the formation of advanced glycation end products (AGEs) and their cross-linking with collagen in vitro and in streptozotocin-induced diabetic rats.

Results: An in vitro assay for the glycation of bovine serum albumin by methylglyoxal showed that GS-E3D inhibited AGE formation at an IC50 value of 19.65 ± 4.35 μg/mL. In addition, GS-E3D showed a potent inhibitory effect (IC50 = 0.42 ± 0.08 mg/mL) on the cross-linking of AGEs with collagen. However, GS-E3D showed no effect on preformed AGEs cross-linked with collagen in the breakdown assay. To determine whether GS-E3D inhibits AGE formation and their cross-linking with proteins in vivo, streptozotocin induced diabetic rats were treated with GS-E3D (25, 50, and 100 mg/kg/day) for 6 weeks. The administration of GS-E3D decreased serum levels of AGEs and their cross linking with proteins in diabetic rats.

Conclusion: The inhibitory effects of this agent on advanced glycation in vitro and in vivo suggested that it may have a potential therapeutic role in controlling diabetes-induced AGE burden in various tissues.

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