title: Protective effects of oxymatrine on experimental diabetic nephropathy.
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.
authors.affiliation: State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, P. R. China.
authors.forename: Changrun
authors.initials: C
authors.lastname: Guo
authors.affiliation: State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, P. R. China.
authors.forename: Fengyu
authors.initials: F
authors.lastname: Han
authors.affiliation: State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, P. R. China.
authors.forename: Chunfeng
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Jiangsu Kanion Pharmaceutical Co., Ltd., Lianyungang, P. R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Xiao
authors.affiliation: State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, P. R. China.
authors.forename: Zhonglin
authors.initials: Z
authors.lastname: Yang
mesh_terms: D000419:Albuminuria / Q000517:prevention & control; D000470:Alkaloids / Q000493:pharmacokinetics / Q000627:therapeutic use*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001806:Blood Urea Nitrogen; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000188:drug therapy; D003928:Diabetic Nephropathies / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D017127:Glycation End Products, Advanced / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007678:Kidney Glomerulus / Q000187:drug effects / Q000473:pathology; D007684:Kidney Tubules / Q000187:drug effects / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D011507:Proteinuria / Q000517:prevention & control; D011807:Quinolizines / Q000493:pharmacokinetics / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D029909:Sophora / Q000737:chemistry*; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D000093842:Matrines
chemical_list: D000470:Alkaloids; D001786:Blood Glucose; D055513:Connective Tissue Growth Factor; D003404:Creatinine; D016207:Cytokines; D017127:Glycation End Products, Advanced; D010936:Plant Extracts; D011807:Quinolizines; D053773:Transforming Growth Factor beta1; C037573:oxymatrine; D000093842:Matrines