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补锌通过调节晶状体蛋白和多元醇途径改善实验性大鼠糖尿病性白内障。

Zinc Supplementation Ameliorates Diabetic Cataract Through Modulation of Crystallin Proteins and Polyol Pathway in Experimental Rats.

机构信息

Department of Biochemistry, CSIR - Central Food Technological Research Institute, Mysore, 570 020, India.

出版信息

Biol Trace Elem Res. 2019 Jan;187(1):212-223. doi: 10.1007/s12011-018-1373-3. Epub 2018 May 13.

DOI:10.1007/s12011-018-1373-3
PMID:29756175
Abstract

Non-enzymatic glycation of lens proteins and elevated polyol pathway in the eye lens have been the characteristic features of a diabetic condition. We have previously reported the benefits of zinc supplementation in reducing hyperglycemia and associated metabolic abnormalities and oxidative stress in diabetic rats. The current study explored whether zinc supplementation protects against cataractogenesis through modulation of glycation of lens proteins, elevated polyol pathway, oxidative stress, and proportion of different heat shock proteins in the eye lens of diabetic rats. Streptozotocin-induced diabetic rats were fed with a zinc-enriched diet (5 and 10 times of normal) for 6 weeks. Supplemental zinc alleviated the progression and maturation of diabetes-induced cataract. Zinc was also effective in preventing the reduced content of total and imbalanced proportion of soluble proteins in the lens. Supplemental zinc also alleviated cross-linked glycation and concomitant expression of the receptor of glycated products and oxidative stress indicators in the eye lens. Zinc supplementation further induced the concentration of heat shock protein in the eye lens of diabetic rats, specifically α-crystallin. Zinc supplementation counteracted the elevated activity and expression of polyol pathway enzymes and molecules in the lens. The results of this animal study endorsed the advantage of zinc supplementation in exerting the antiglycating influence and downregulating polyol pathway enzymes to defer cataractogenesis in diabetic rats.

摘要

晶状体蛋白的非酶糖基化和眼晶状体中多元醇途径的升高是糖尿病的特征。我们之前曾报道过锌补充剂在降低高血糖和相关代谢异常以及糖尿病大鼠的氧化应激方面的益处。本研究探讨了锌补充是否通过调节晶状体蛋白的糖化、升高的多元醇途径、氧化应激以及眼晶状体中不同热休克蛋白的比例来预防糖尿病大鼠的白内障形成。用富含锌的饮食(正常饮食的 5 倍和 10 倍)喂养链脲佐菌素诱导的糖尿病大鼠 6 周。补充锌可缓解糖尿病诱导的白内障的进展和成熟。锌还可有效预防晶状体中总可溶性蛋白含量降低和比例失衡。补充锌还可减轻交联糖基化以及糖基化产物受体和眼晶状体中氧化应激指标的伴随表达。锌补充进一步诱导了糖尿病大鼠眼晶状体中热休克蛋白的浓度,特别是α-晶体蛋白。锌补充可拮抗晶状体中多元醇途径酶和分子的升高活性和表达。这项动物研究的结果证实了锌补充在发挥抗糖化作用和下调多元醇途径酶以延缓糖尿病大鼠白内障形成方面的优势。

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