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虾青素在2型糖尿病和糖尿病视网膜病变模型中抑制醛糖还原酶活性。

Astaxanthin inhibits aldose reductase activity in , a model of type 2 diabetes and diabetic retinopathy.

作者信息

Benlarbi-Ben Khedher Maha, Hajri Khouloud, Dellaa Ahmed, Baccouche Basma, Hammoum Imane, Boudhrioua-Mihoubi Nourhene, Dhifi Wissal, Ben Chaouacha-Chekir Rafika

机构信息

Laboratory of Physiopathology, Food and Biomolecules (PAB): LR17ES03 The High Institute of Biotechnology of Sidi Thabet (ISBST) University of Manouba (UMA) Sidi Thabet Tunisia.

出版信息

Food Sci Nutr. 2019 Nov 12;7(12):3979-3985. doi: 10.1002/fsn3.1259. eCollection 2019 Dec.

DOI:10.1002/fsn3.1259
PMID:31890176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6924305/
Abstract

Astaxanthin (ATX) is a marine carotenoid known for its powerful antioxidant and neuroprotective properties. In this study, we investigated the in vitro and in vivo potential inhibitory effect of ATX on the aldose reductase (AR) activity, a key enzyme in the polyol pathway responsible for the pathogenesis of diabetic complications including diabetic retinopathy (DR). The gerbil (), an animal model for type 2 diabetes and DR has been used. The erythrocyte and retinal AR activity of individuals were, respectively, assessed monthly and at the 7th month during a 7-month hypercaloric diet (HD) using a NADPH oxidation method. Meanwhile, the body weight and blood glucose of the gerbils were monitored. After 7 months, individuals were fed with ATX (4.8 mg/kg of body weight) once a day for 1 week. The results showed that the HD-fed animals developed significant obesity and hyperglycemia in comparison with controls. Erythrocyte AR activity showed a progressive and significant increase in the HD-fed group compared with controls. Retinal AR activity was higher in the 7-month HD-fed group compared with controls. Erythrocyte AR activity was markedly decreased after ATX-treatment in vitro and in vivo. These findings suggested that ATX inhibited the erythrocyte AR activity and could be used for DR prevention and/or early treatment.

摘要

虾青素(ATX)是一种海洋类胡萝卜素,以其强大的抗氧化和神经保护特性而闻名。在本研究中,我们研究了ATX对醛糖还原酶(AR)活性的体外和体内潜在抑制作用,醛糖还原酶是多元醇途径中的关键酶,负责包括糖尿病视网膜病变(DR)在内的糖尿病并发症的发病机制。本研究使用了沙土鼠(一种2型糖尿病和DR的动物模型)。在为期7个月的高热量饮食(HD)期间,分别每月和第7个月使用NADPH氧化法评估个体的红细胞和视网膜AR活性。同时,监测沙土鼠的体重和血糖。7个月后,给个体每天一次喂食ATX(4.8mg/kg体重),持续1周。结果表明,与对照组相比,接受HD喂养的动物出现了明显的肥胖和高血糖。与对照组相比,HD喂养组的红细胞AR活性呈渐进性显著增加。7个月HD喂养组的视网膜AR活性高于对照组。体外和体内ATX处理后,红细胞AR活性显著降低。这些发现表明,ATX抑制红细胞AR活性,可用于DR的预防和/或早期治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/af3af26a2313/FSN3-7-3979-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/01040492e4da/FSN3-7-3979-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/6a242b706e78/FSN3-7-3979-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/d580dcfb7acf/FSN3-7-3979-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/83163e5aa44d/FSN3-7-3979-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/7e3b8a6f5fbc/FSN3-7-3979-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/af3af26a2313/FSN3-7-3979-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/01040492e4da/FSN3-7-3979-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/6a242b706e78/FSN3-7-3979-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/d580dcfb7acf/FSN3-7-3979-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/83163e5aa44d/FSN3-7-3979-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/7e3b8a6f5fbc/FSN3-7-3979-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/358b/6924305/af3af26a2313/FSN3-7-3979-g006.jpg

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