Renal expression of Bach1 and oxidative stress in chronic kidney disease: evidence from a preclinical model.

INTRODUCTION

The transcription factor BTB and CNC homology 1 (Bach1) represses the nuclear factor erythroid 2-related factor 2 (Nrf2), which controls antioxidant gene expression, and its role in chronic kidney disease (CKD) remains unclear.

METHODS

CKD was induced by 5/6 nephrectomy in rats. Kidney fibrosis and oxidative stress markers were measured. The gene expression of Nrf2, Bach1, and nuclear factor kappa B (NF-κB) was assessed.

RESULTS

CKD increased oxidative stress markers in plasma, kidney, and heart, as well as promoted kidney fibrosis. Moreover, CKD reduced cardiac Nrf2 expression. However, Bach1, Nrf2, and NF-κB remained unchanged in the kidney.

CONCLUSION

CKD did not modulate Bach1 mRNA levels in the kidneys of 5/6 nephrectomized rats.