Center of Aging Research, China Medical University Hospital, Taichung City, Taiwan.
Mol Nutr Food Res. 2014 Jul;58(7):1426-35. doi: 10.1002/mnfr.201300910. Epub 2014 Mar 3.
Antiglycative effects of glycyrrhizic acid (GA) in kidney of diabetic mice were examined.
GA at 0.05, 0.1, and 0.2% was supplied to diabetic mice for 9 wk. Results showed that GA intake increased its deposit in kidney, raised plasma insulin level, decreased plasma glucose and blood urine nitrogen levels, and improved creatinine clearance rate (p < 0.05). GA intake dose-dependently reduced renal carboxymethyllysine level, and at 0.1 and 0.2% decreased plasma HbA1c, urinary glycated albumin, and renal pentosidine levels (p < 0.05). Dietary GA intake declined renal aldose reductase activity and protein expression, as well as lowered renal fructose and sorbitol levels (p < 0.05). GA intake dose-dependently increased glyoxalase-1 activity and expression, and decreased renal methylglyoxal level (p < 0.05). This compound at 0.1 and 0.2% raised glyoxalase-2 activity and protein expression, and increased d-lactate formation (p < 0.05). GA intake dose-dependently suppressed renal expression of nuclear factor kappa B (NF-κB) p65 and p-p38, decreased reactive oxygen species production, and retained glutathione content (p < 0.05). This compound at 0.1 and 0.2% downregulated renal expression of NF-κB p50 and p-ERK1/2 (p < 0.05), and lowered renal level of monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1).
These findings suggest that glycyrrhizic acid is an antiglycative and renal-protective agent.
研究了甘草酸（GA）在糖尿病小鼠肾脏中的抗糖化作用。
将 0.05%、0.1%和 0.2%的 GA 供给糖尿病小鼠 9 周。结果表明，GA 摄入增加了其在肾脏中的沉积，提高了血浆胰岛素水平，降低了血浆葡萄糖和血尿素氮水平，并改善了肌酐清除率（p<0.05）。GA 摄入剂量依赖性地降低了肾脏羧甲基赖氨酸水平，并且在 0.1%和 0.2%时降低了血浆 HbA1c、尿糖化白蛋白和肾脏戊糖含量（p<0.05）。膳食 GA 摄入降低了肾脏醛糖还原酶活性和蛋白表达，以及降低了肾脏果糖和山梨醇水平（p<0.05）。GA 摄入剂量依赖性地增加了糖氧还蛋白-1 活性和表达，并降低了肾脏甲基乙二醛水平（p<0.05）。该化合物在 0.1%和 0.2%时提高了糖氧还酶-2 活性和蛋白表达，并增加了 d-乳酸的形成（p<0.05）。GA 摄入剂量依赖性地抑制了肾脏核因子-κB（NF-κB）p65 和 p-p38 的表达，减少了活性氧的产生，并保留了谷胱甘肽含量（p<0.05）。该化合物在 0.1%和 0.2%时下调了肾脏 NF-κB p50 和 p-ERK1/2 的表达，并降低了肾脏单核细胞趋化蛋白-1（MCP-1）和细胞间黏附分子-1（ICAM-1）的水平。
这些发现表明，甘草酸是一种抗糖化和肾脏保护剂。
