Improvement effects of puerarin on glycated brain damages in rats induced by D-galactose.
- Author:
Jun-Hua LV
1
;
Shi-Ping ZHANG
;
Fei-Hai SHEN
;
Jing-Qiange PAN
;
Hai-Rong TAN
Author Information
- Publication Type:Journal Article
- MeSH: Aldehyde Reductase; metabolism; Animals; Brain; metabolism; pathology; Calcium; metabolism; Erythrocytes; enzymology; Female; Fructosamine; blood; Galactose; antagonists & inhibitors; Glycated Hemoglobin A; metabolism; Glycation End Products, Advanced; metabolism; Hippocampus; ultrastructure; Isoflavones; isolation & purification; pharmacology; Male; Mitochondria; ultrastructure; Neuroprotective Agents; pharmacology; Plants, Medicinal; chemistry; Pueraria; chemistry; Random Allocation; Rats; Rats, Sprague-Dawley
- From: China Journal of Chinese Materia Medica 2006;31(14):1184-1187
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the improvement effects of puerarin on glycated brain damages in rat model induced by D-galactose.
METHODThe model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks, and all rats were treated with puerarin (high dose 300 mg x kg(-1), middle dose 150 mg x kg(-1), low dose 75 mg x kg(-1)) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products (fructosamine in serum, glycohaemoglobin, advanced glycation end-products) and AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope.
RESULTHigh dose and middle dose of puerarin can decrease the activity of aldose reductase in red blood cells (P < 0.01), and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P < 0.01). Also, puerarin can decrease the content of AGEs in brain and the level of calcium ions in brain cells (P < 0.05, P < 0.01), and decrease lesions degree in mitochondria in brain hippocampus cells.
CONCLUSIONPuerarin can produce the protective effects on glycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.
