MO565: Evaluation of Bach1 Mrna Expression (Repressor of NRF2) in Patients With Chronic Kidney Disease
Autor: | Denise Mafra, Livia Alvarenga, Beatriz G. Baptista, Susane Fanton, Marcia M. Ribeiro, Bruna R. Paiva, Liana Trugilho, Ludmila Cardozo |
---|---|
Rok vydání: | 2022 |
Předmět: | |
Zdroj: | Nephrology Dialysis Transplantation. 37 |
ISSN: | 1460-2385 0931-0509 |
DOI: | 10.1093/ndt/gfac074.010 |
Popis: | BACKGROUND AND AIMS BTB and CNC homology 1 (Bach1) is a protein into the cells that antagonizes the actions of nuclear factor erythroid 2-related factor-2 (Nrf2), a master regulator of cytoprotective responses. Bach1 binds to genomic DNA and can inhibit the synthesis of antioxidant enzymes, increasing inflammation. Bach1 may be a therapeutic target to mitigate inflammation in patients with chronic kidney disease (CKD). However, no clinical study has been reported on Bach1 in patients with CKD. This study aimed to evaluate Bach1 mRNA expression in different treatments of CKD, including patients on conservative treatment (non-dialysis), hemodialysis (HD) and peritoneal dialysis (PD). METHODS Twenty patients on HD (54.3 ± 13.7 years old, nine men), fifteen on PD (51.4 ± 14.9 years old, eight men) and thirteen non-dialysis patients (61.0 ± 6.9 years old, seven men, estimated glomerular filtration rate of 39.2 ± 9.6 mL/min/1.73 m2) were enrolled in the study. The peripheral blood mononuclear cells were isolated and processed to evaluate the expression of nuclear factor-kB (NF-kB), Nrf2 and Bach1 by quantitative real-time polymerase chain reaction. Malondialdehyde (MDA), a lipid peroxidation marker, and C-reactive protein (CRP) plasma levels were also measured. RESULTS Bach1 mRNA expression was significantly higher in patients on hemodialysis (P CONCLUSION Patients with CKD on HD patients seem to have upregulation of Bach1 mRNA expression compared to patients on conservative and DP treatment. The associations among Nrf2 and Bach1 expressions in these patients deserve further investigation. |
Databáze: | OpenAIRE |
Externí odkaz: |