title: Diosgenin attenuates vascular calcification in chronic renal failure rats.
abstract: Vascular calcification due to elevated phosphate levels is the major contributor of cardiovascular dysfunction. The oxidative stress and gene expression events modulate the transdifferentiation of vascular smooth muscle cells into osteogenic phenotype. This present study intends to evaluate the dose-dependent effect of diosgenin, an antioxidant on high phosphate induced vascular calcification in adenine-induced chronic renal failure rats. High phosphate environment causes elevated calcium accumulation with related histological changes and alkaline phosphatase activity in aorta. Further it downregulates the activity of enzymatic antioxidants and elevates the level of lipid peroxidative markers. Moreover, the renal failure leads to reduced nitric oxide production. But, treatment with diosgenin at a dose of 10, 20, and 40 mg/kg given via oral gavages causes reversion of all the above events in a dose-dependent manner. The highest dose has shown more potential activity than other two doses, which has the ability to protect the alteration of liver markers and red blood cell antioxidant system without any adverse effects and it does not alter the kidney associated changes too. Finally, the Fourier transform infrared spectroscopy study strongly supports its ability to protect the macromolecules from oxidative stress. All the above evidences show that diosgenin has overall benefits against renal failure-induced vascular calcification-associated oxidative stress.
authors: Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamilnadu, India.
authors: Jeganathan
authors: J
authors: Manivannan
authors: T R
authors: TR
authors: Barathkumar
authors: Jeganathan
authors: J
authors: Sivasubramanian
authors: Pandian
authors: P
authors: Arunagiri
authors: Boobalan
authors: B
authors: Raja
authors: Elumalai
authors: E
authors: Balamurugan
mesh_terms: D000225:Adenine; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001011:Aorta / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D015415:Biomarkers / Q000097:blood; D002118:Calcium / Q000097:blood; D002374:Catalase / Q000378:metabolism; D004144:Diosgenin / Q000494:pharmacology* / Q000627:therapeutic use; D004353:Drug Evaluation, Preclinical; D004912:Erythrocytes / Q000201:enzymology; D005979:Glutathione Peroxidase / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D015227:Lipid Peroxidation; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D010758:Phosphorus / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D017550:Spectroscopy, Fourier Transform Infrared; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D061205:Vascular Calcification / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D010758:Phosphorus; D009569:Nitric Oxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D000469:Alkaline Phosphatase; D000225:Adenine; D004144:Diosgenin; D002118:Calcium