Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Nutr Food Res. 2014 Jul;58(7):1426-35. doi: 10.1002/mnfr.201300910. Epub 2014 Mar 3.

Glycyrrhizic acid attenuated glycative stress in kidney of diabetic mice through enhancing glyoxalase pathway.

Author information

1
Center of Aging Research, China Medical University Hospital, Taichung City, Taiwan.

Abstract

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.

KEYWORDS:

Diabetic nephropathy; Glycation; Glycyrrhizic acid; Glyoxalase-1; Methylglyoxal

PMID:
24585461
DOI:
10.1002/mnfr.201300910
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center