Abstract
BackgroundChronic kidney disease (CKD) is a worldwide public health problem affecting 10% of the adult population. One of the most important factors in the progression of CKD from early stages is oxidative stress. Currently there is limited efficacy to treat this problem so the objective of this study was to test Epicatechin (Epi), effects in a mice model of CKDMethodsA nephrectomy 5/6 (Nf) in C‐57BL6 mice model was implemented and Epi treatment (14 days doses doses of 0.01, 0.1 and 1 mg/kg) was provided by gavage. Changes in Systolic blood pressure (SBP), serum urea and creatinine, renal cortex morphology, serum tetrahydrobiopterin (BH4), in 3‐nitrotyrosine as oxidative damage marker and of Angiotensin II AT1 receptor (AGTR1) and NOX‐4 protein expression were evaluatedResultsSBP increased in the Nf group and decrease significantly in Nf+ Epi groups. Serum urea and creatinine levels increased in the Nf group Epi treatment induced a significant decrease. Epi treatment induced a dose dependent increase in serum BH4 in Nf animals. Normal renal cortex morphology was conserved at 1 m/kg Epi dose. The expression of AGTR1 and NOX‐4 was increased in the Nf group, Epi treatment in a dose dependent manner decrease the AGTR1 and NOX‐4 expression.ConclusionThe present findings suggest that Epi could prevent the progression of CKD and may be used as complement for the modulation of blood pressure and f renal dysfunction.Support or Funding InformationConacyt 253769This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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