Kim Chan-Sik, Jo Kyuhyung, Pyo Mi-Kyung, Kim Jin Sook, Kim Junghyun
Korean Medicine Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
International Ginseng and Herb Research Institute, Geumsan, Republic of Korea.
J Exerc Nutrition Biochem. 2017 Jun 30;21(2):56-62. doi: 10.20463/jenb.2017.0011.
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.
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.
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.
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.
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。
在本研究中,我们评估了GS-E3D在体外以及在链脲佐菌素诱导的糖尿病大鼠体内对晚期糖基化终产物(AGEs)形成及其与胶原蛋白交联的抑制作用。
通过甲基乙二醛对牛血清白蛋白进行糖基化的体外试验表明,GS-E3D以19.65±4.35μg/mL的IC50值抑制AGEs的形成。此外,GS-E3D对AGEs与胶原蛋白的交联显示出强效抑制作用(IC50 = 0.42±0.08mg/mL)。然而,在分解试验中,GS-E3D对与胶原蛋白交联的预先形成的AGEs没有影响。为了确定GS-E3D在体内是否抑制AGEs的形成及其与蛋白质的交联,用GS-E3D(25、50和100mg/kg/天)治疗链脲佐菌素诱导的糖尿病大鼠6周。GS-E3D的给药降低了糖尿病大鼠血清中AGEs的水平及其与蛋白质的交联。
该药物在体外和体内对晚期糖基化的抑制作用表明,它可能在控制糖尿病诱导的各种组织中的AGE负担方面具有潜在的治疗作用。