title: Beneficial effect of genistein on lowering blood pressure and kidney toxicity in fructose-fed hypertensive rats.
abstract: The study evaluates the effects of genistein on blood pressure (BP) and ultrastructural changes in kidney of fructose-fed hypertensive rats. Male Wistar rats were fed a diet containing 60 % starch or 60 % fructose as the source of carbohydrate. After 15 d, rats in each dietary group were divided into two groups and were treated with either genistein (1 mg/kg per d) in dimethylsulfoxide (DMSO) or 30 % DMSO alone. BP, pressor mechanisms, protein kinase C-βII (PKC-βII) expression, endothelial NO synthase (eNOS) expression and renal ultrastructural changes were evaluated after 60 d. Fructose-fed rats displayed significant elevation in BP and heart rate. Significant increase in plasma angiotensin-converting enzyme (ACE) activity, alterations in renal lipid profile, nitrite and kallikrein activity, enhanced expression of membrane-associated PKC-βII and decreased expression of eNOS were observed in them. Histology and electron microscopic studies showed structural changes in the kidney. Genistein administration lowered BP, restored ACE, PKC-βII and eNOS expression and preserved renal ultrastructural integrity. These findings demonstrate that genistein has effects on eNOS activity in renal cells, leading to eNOS activation and NO synthesis. These effects could have been mediated by activation of PKC-βII. The observed benefits of genistein make it a promising candidate for therapy of diabetic kidney disease.
authors.affiliation: Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar 608 002, Tamil Nadu, India. nalpybiochem@gmail.com
authors.forename: Nallasamy
authors.initials: N
authors.lastname: Palanisamy
authors.forename: Anuradha C
authors.initials: AC
authors.lastname: Venkataraman
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects*; D003928:Diabetic Nephropathies / Q000139:chemically induced / Q000188:drug therapy; D004032:Diet; D019422:Dietary Sucrose / Q000009:adverse effects; D005632:Fructose / Q000009:adverse effects*; D019833:Genistein / Q000494:pharmacology / Q000627:therapeutic use*; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism; D007610:Kallikreins / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D011493:Protein Kinase C / Q000378:metabolism; D064546:Protein Kinase C beta; D051381:Rats; D017208:Rats, Wistar; D013025:Glycine max / Q000737:chemistry
chemical_list: D000959:Antihypertensive Agents; D019422:Dietary Sucrose; D009573:Nitrites; D010936:Plant Extracts; D005632:Fructose; D009569:Nitric Oxide; D019833:Genistein; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D011493:Protein Kinase C; D064546:Protein Kinase C beta; D007703:Peptidyl-Dipeptidase A; D007610:Kallikreins