Study on the protective effect of ursolic acid on alloxan-induced diabetic renal injury and its underlying mechanisms.
- Author:
Min-You QI
1
;
Jun-Jie YANG
;
Bin ZHOU
;
Ding-Yi PAN
;
Xian SUN
Author Information
- Publication Type:Journal Article
- MeSH: Alloxan; adverse effects; Animals; Antioxidants; metabolism; Blood Glucose; Blood Urea Nitrogen; Creatinine; metabolism; Diabetes Mellitus, Experimental; physiopathology; Diabetic Nephropathies; chemically induced; drug therapy; Interleukin-6; metabolism; Kidney; physiopathology; Male; Mice; Superoxide Dismutase; metabolism; Triterpenes; pharmacology; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Applied Physiology 2014;30(5):445-448
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of ursolic acid (UA) on the alloxan-induced kidney injury in diabetic mice and explored its possible mechanisms.
METHODSDiabetes mellitus was induced in male Kunming mice by an injection of alloxan (70 mg/kg, i.v.). After 72 hours, blood glucose levels were detected and mice with blood glucose levels over 13.9 mmol/L were considered as diabetic and selected for further experiment. Thirty mice were randomly divided into three groups: control, diabetic and diabetic + UA(35 mg/kg/d, i.g. continuously for 8 weeks). Blood glucose concentration, organ coefficient of kidney, blood urea nitrogen (BUN), creatinine (Cr) as well as renal tissue levels of superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined. Pathology of the renal tissue was measured by hematoxylin-eosin staining.
RESULTSCompared to the control group, blood glucose, organ coefficient of kidney, BUN and Cr increased significantly. In addition, SOD activities was reduced markedly and levels of MDA and inflammatory factors (TNF-α, IL-6) increased significantly. Renal cells from model group rats showed atrophy and disordered after HE staining and infiltration of inflammatory cells also appeared in renal tissue of the model group. These changes were significantly attenuated in the diabetic group treated with UA.
CONCLUSIONUA can significantly relieve renal damage in mice with diabetic nephropathy induced by alloxan, which might be related to decreased blood glucose level, antioxidation effect and inhibiting the production of inflammatory factors such as TNF-α and IL-6.