Abstract
Diabetic nephropathy, one of the most common and serious vascular complications of
both type 1
and type 2 diabetes mellitus, has become a major contributor of end-stage renal failure.
The
aims of this study were to investigate the effects and possible underlying action
mechanism(s)
of oxymatrine on renal damage in diabetic rats. Diabetes was induced in male Sprague-Dawley
rats
by administering a high-fat diet and an intraperitoneal 30 mg/kg streptozotocin injection.
The
animals were treated orally with saline, metformin hydrochloride, and oxymatrine at
50, 100, and
150 mg/kg/day for 11 weeks. At the end of the treatment, renal tissue, blood, and
urine samples
were collected for histological and biochemical examination. The results revealed
that
oxymatrine significantly decreased blood glucose, urinary protein and albumin excretion,
serum
creatinine, and blood urea nitrogen in diabetic rats, and ameliorated diabetes-induced
glomerular and tubular pathological changes. Furthermore, oxymatrine significantly
prevented
oxidative stress and reduced the contents of renal advanced glycation end products,
transforming
growth factor-β1, connective tissue growth factor, and inflammatory cytokines in diabetic
rats. All these results indicate that oxymatrine has protective effects on experimental
diabetic
nephropathy by multiple mechanisms.
Key words
oxymatrine - diabetic nephropathy - oxidative stress - TNF-
α
- TGF-
β1 -
Sophora flavescens
- Fabaceae
