title: Boldine prevents renal alterations in diabetic rats.
abstract: Diabetic nephropathy alters both structure and function of the kidney. These alterations are associated with increased levels of reactive oxygen species, matrix proteins, and proinflammatory molecules. Inflammation decreases gap junctional communication and increases hemichannel activity leading to increased membrane permeability and altering tissue homeostasis. Since current treatments for diabetic nephropathy do not prevent renal damage, we postulated an alternative treatment with boldine, an alkaloid obtained from boldo with antioxidant, anti-inflammatory, and hypoglycemic effects. Streptozotocin-induced diabetic and control rats were treated or not treated with boldine (50 mg/Kg/day) for ten weeks. In addition, mesangial cells were cultured under control conditions or in high glucose concentration plus proinflammatory cytokines, with or without boldine (100 µmol/L). Boldine treatment in diabetic animals prevented the increase in glycemia, blood pressure, renal thiobarbituric acid reactive substances and the urinary protein/creatinine ratio. Boldine also reduced alterations in matrix proteins and markers of renal damage. In mesangial cells, boldine prevented the increase in oxidative stress, the decrease in gap junctional communication, and the increase in cell permeability due to connexin hemichannel activity induced by high glucose and proinflammatory cytokines but did not block gap junction channels. Thus boldine prevented both renal and cellular alterations and could be useful for preventing tissue damage in diabetic subjects.
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
authors.forename: Romina
authors.initials: R
authors.lastname: Hernández-Salinas
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
authors.forename: Alejandra Z
authors.initials: AZ
authors.lastname: Vielma
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
authors.forename: Marlene N
authors.initials: MN
authors.lastname: Arismendi
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
authors.forename: Mauricio P
authors.initials: MP
authors.lastname: Boric
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile ; Instituto Milenio, Centro Interdisciplinario de Neurociencias de Valparaíso, Valparaíso, Chile.
authors.forename: Juan C
authors.initials: JC
authors.lastname: Sáez
authors.affiliation: Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O'Higgins, No. 340, 6513677 Santiago, Chile.
authors.forename: Victoria
authors.initials: V
authors.lastname: Velarde
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001060:Aporphines / Q000627:therapeutic use*; D002478:Cells, Cultured; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D003928:Diabetic Nephropathies / Q000503:physiopathology / Q000517:prevention & control*; D004353:Drug Evaluation, Preclinical; D007677:Kidney Function Tests; D008297:Male; D031611:Peumus; D010936:Plant Extracts / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D001060:Aporphines; D010936:Plant Extracts; C011686:boldine