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原儿茶酸对糖尿病小鼠肾脏的抗糖化作用。

Antiglycative effects of protocatechuic acid in the kidneys of diabetic mice.

机构信息

Department of Health and Nutrition Biotechnology, Asia University, Taichung City, Taiwan.

出版信息

J Agric Food Chem. 2011 May 11;59(9):5117-24. doi: 10.1021/jf200103f. Epub 2011 Apr 1.

DOI:10.1021/jf200103f
PMID:21456600
Abstract

Protocatechuic acid (PCA) at 2 or 4% was supplied to diabetic mice for 12 weeks. PCA treatments increased its deposit in organs and significantly reduced the plasma HbA1c level, the urinary glycative albumin level, and renal production of carboxymethyllysine (CML), pentosidine, sorbitol, and fructose (p < 0.05). However, PCA treatments only at 4% significantly decreased brain content of CML, pentosidine, fructose, and sorbitol (p < 0.05). PCA treatments at 2 and 4% significantly lowered renal activity and mRNA expression of aldose reductase and sorbitol dehydrogenase (p < 0.05), and PCA treatments only at 4% significantly enhanced renal glyoxalase I mRNA expression (p < 0.05). PCA treatments also dose-dependently decreased the renal level of type-IV collagen, fibronectin, and transforming growth factor-β1 (p < 0.05), as well as dose-dependently diminished renal protein kinase C (PKC) activity (p < 0.05); however, PCA treatments only at 4% suppressed renal mRNA expression of PKC-α and PKC-beta (p < 0.05). PCA treatments at 4% significantly restored renal mRNA expression of peroxisome proliferator-activated receptor (PPAR)-α and PPAR-γ, as well as suppressed expression of the advanced glycation end-product receptor (p < 0.05). These findings suggest that the supplement of PCA might be helpful for the prevention or alleviation of glycation-associated diabetic complications.

摘要

原儿茶酸(PCA)以 2%或 4%的浓度供给糖尿病小鼠 12 周。PCA 处理增加了其在器官中的沉积,并显著降低了血浆 HbA1c 水平、尿糖基化白蛋白水平以及肾脏产生的羧甲基赖氨酸(CML)、戊糖、山梨醇和果糖(p<0.05)。然而,只有 4%的 PCA 处理显著降低了脑内 CML、戊糖、果糖和山梨醇的含量(p<0.05)。2%和 4%的 PCA 处理均显著降低了醛糖还原酶和山梨醇脱氢酶的肾脏活性和 mRNA 表达(p<0.05),而只有 4%的 PCA 处理显著增强了肾脏糖氧还蛋白 I 的 mRNA 表达(p<0.05)。PCA 处理还呈剂量依赖性地降低了肾脏 IV 型胶原、纤维连接蛋白和转化生长因子-β1 的水平(p<0.05),以及剂量依赖性地降低了肾脏蛋白激酶 C(PKC)活性(p<0.05);然而,只有 4%的 PCA 处理抑制了肾脏 PKC-α和 PKC-β的 mRNA 表达(p<0.05)。4%的 PCA 处理显著恢复了肾脏过氧化物酶体增殖物激活受体(PPAR)-α和 PPAR-γ的 mRNA 表达,并抑制了晚期糖基化终产物受体的表达(p<0.05)。这些发现表明,PCA 的补充可能有助于预防或缓解糖基化相关的糖尿病并发症。

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