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

IF 1.6 Q3 UROLOGY & NEPHROLOGY

Jornal brasileiro de nefrologia : 'orgao oficial de Sociedades Brasileira e Latino-Americana de Nefrologia Pub Date : 2026-07-01 DOI:10.1590/2175-8239-JBN-2025-0333en

Beatriz Oliveira Da Cruz, Patricia Pereira Almeida, Nathalia Silva-Costa, Michele Lima Brito, D'Angelo Carlo Magliano, Milena Barcza Stockler-Pinto

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Abstract

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.

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慢性肾病患者肾脏中Bach1表达与氧化应激：来自临床前模型的证据

转录因子BTB和CNC同源1 （Bach1）抑制核因子红系2相关因子2 (Nrf2)，而Nrf2控制抗氧化基因的表达，其在慢性肾脏疾病（CKD）中的作用尚不清楚。方法：采用大鼠5/6肾切除术诱导CKD。测定肾纤维化和氧化应激指标。检测Nrf2、Bach1、核因子κB （NF-κB）基因表达。结果：CKD增加血浆、肾脏和心脏的氧化应激标志物，并促进肾纤维化。此外，CKD降低了心脏Nrf2的表达。然而，Bach1、Nrf2和NF-κB在肾脏中保持不变。结论：CKD不影响5/6肾切除大鼠肾脏Bach1 mRNA水平。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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