Scope
Antiglycative effects of glycyrrhizic acid (GA) in kidney of diabetic mice were examined.
Methods and results
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).
Conclusions
These findings suggest that glycyrrhizic acid is an antiglycative and renal‐protective agent.